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Researcher Tom Cappola tells us about the latest clinical trials and medical breakthroughs to be announced during Scientific Sessions.

Chief of the cardiovascular medicine division in the Perelman School of Medicine at the University of Pennsylvania, Tom Cappola.

For the first time in its near 100-year history, the American Heart Association (AHA)will host its annual meeting in Philadelphia. AHAs Scientific Sessions is the largest cardiovascular meeting in the United States. On November 16-18, the meeting will attract nearly 18,000 attendees from more than 100 countries to the Pennsylvania Convention Center, and an additional two million medical professionals who will participate virtually in lectures and discussions about basic, translational, clinical and population science innovations aimed at reducing disability and deaths caused by cardiovascular disease and stroke.

The American Heart Association is excited to be in Philadelphia, said Michelle Kirkwood, director of National Science Media Relations for AHA. It has been on our wish list for some time, especially since the renovations at the Pennsylvania Convention Center and the citys landmark, robust nonsmoking laws that align directly with the American Heart Associations health and wellness goals. We are excited for our thousands of attendees to visit Philadelphia.

More than 610,000 people die of heart disease in the United States every year, according to the CDC. While heart disease is a leading cause of death for both men and women, it claims the lives of over 400,000 American women each year, or one death every 80 seconds. During the three-day meeting, more than 12,000 leading physicians, scientists, cardiologists and healthcare professionals in the global cardiovascular health community will host 850 educational sessions and more than 4,100 original research presentations to unveil the late-breaking science, clinical trials, and novel therapeutics and pathways that are shaping the future of cardiovascular care.

Its very fitting for Scientific Sessions to be here, chief of the cardiovascular medicine division in the Perelman School of Medicine at the University of Pennsylvania Tom Cappola said. We have the first medical school in the country and the first teaching hospital in the country. It makes sense that these new innovations would be presented in a place where theres already been so much innovation.

Cappola will be one of several Penn researchers leading the Cardiovascular Expert Theater, Innovations in Cardiovascular Therapies session during the meeting. Here are just a few big trends in heart care that Cappola says we can expect to learn more about during this weekends meeting:

Using artificial intelligence to monitor heart health

Artificial intelligence (AI) is having a big impact on cardiovascular care. Results from two preliminary studies to be presented this weekend will show AI can be used to accurately examine electrocardiogram (ECG) test results to possibly predict irregular heartbeat and risk of death. There will also be a presentation on the Apple Heart Study, which found that the Apple Watch and other wearable remote monitoring devices may be capable of detecting atrial fibrillation (aFib), an irregular and often rapid heartbeat that can lead to blood clots, stroke, heart failure and other complications.

Identifying new risk factors for aFib and stroke

George Mason University researchers will present results from two studies that found young people who smoke marijuana regularly have an increased risk of stroke. According to the study findings, young adults between the ages 18 and 44 who reported frequent use of marijuana, cigarettes and e-cigarettes were three times more likely to suffer stroke than young adults who did not smoke marijuana at all. The study also found that African-American males between the ages of 15 and 24 faced the highest risk of being hospitalized for arrhythmia.

In one Penn study to be presented this weekend, researchers found women who are diagnosed with peripartum cardiomyopathy (PPCM) during late pregnancy or within a month following delivery are more likely to experience restored cardiac function and improved outcomes compared to those who are diagnosed later in the postpartum period. The findings underscore the need for increased awareness and monitoring of heart failure symptoms, particularly among black women, who, on average, are diagnosed significantly later than white patients, according to study results.

Making advances in genetics and genomics

Another big trend at this years meeting will be the continued advancement in genetics and genomics, and how thats impacting cardiovascular care.

I think that genomic medicine has arrived and its arriving in waves, but it will ultimately affect all aspects of cardiovascular care, Cappola said. We have lots of people getting their 23andMe for sort of recreational purposes and they dont know what to do with it. But were starting to figure out what to do with that genetic information to improve care.

Another Penn Medicine study to be presented during the meeting will show why taller people may have an increased risk of developing atrial aFib. The research found a strong link between the genetic variants associated with height and ones risk for AFib, for the first time demonstrating that height may be a causal not correlated risk factor for the condition. Researchers hope insight from human genetics in large studies like this one will help them better understand causal risk factors for common disease.

It takes expertise to find links like this. Thats why researchers go to the American Heart Association meetings. You get all the experts together, they share their knowledge and this helps us to actually figure out what to do with this genetic information, Cappola said. Thats true across the board, but its particularly important for genomic medicine as it continues to advance.

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The American Heart Association's Annual Conference Comes to Philly This Weekend - Philadelphia magazine

SINGAPORE - Sexual orientation cannot be wilfully changed and is a product of genetic and environmental factors, said lawyers arguing for the repeal of Section 377A of the Penal Code.

They argued that the law, which criminalises acts of "gross indecency" between men, violates Article 9 of the Constitution guaranteeing the right to life and personal liberty, and Article 12guaranteeing equal protection before the law.

The legal team, consisting of Mr Eugene Thuraisingam, Mr Suang Wijaya and Mr Johannes Hadi of Eugene Thuraisingam LLP, represented disc jockey Johnson Ong Ming in the High Court on Monday (Nov 18) in the second of three cases to be brought against Section 377A this month.

The Attorney-General's Chambers (AGC) has been listed as the respondent in all of the cases.

Mr Ong's lawyers presented expert evidence from six medical professionals to back up their claims, including three called by Mr Ong and three called by the AGC.

Those called by Mr Ong were British psychiatrist Dinesh Bhugra, a professor of mental health and diversity at the Institute of Psychiatry at King's College London; Dr Jacob Rajesh, a senior consultant psychiatrist at the Promises Clinic in Novena Medical Centre; and American public health and epidemiology professor Chris Beyrer of the Johns Hopkins Bloomberg School of Public Health.

Those called by the AGC were Dr Cai Yiming, an emeritus consultant in the Department of Developmental Psychiatry at the Institute of Mental Health; retired geneticist John Tay Sin Hock, who was the former Head of Division of Human Genetics at the National University of Singapore; and Dr Derrick Heng Mok Kwee, group director of the Public Health Group in the Ministry of Health.

The experts on both sides largely agree that sexual orientation cannot be wilfully changed and that biological factors such as one's genes and non-social environmental factors such as exposure to different levels of hormones in the womb are contributors to one's sexual orientation, the lawyers argued.

There is also no credible scientific evidence that "therapy" aimed at changing sexual orientation, such as reparative or conversion therapy, is safe or effective, they added.

But the experts differed on whether choice and social environmental factors like culture play a role in determining sexual orientation.

Dr Cai said there is "very little we can scientifically conclude about whether there is choice in sexual orientation".

Dr Tay said that genetics may play some part in determining sexual orientation but are not the sole cause of it, suggesting that culture plays a role as well.

Mr Ong's lawyers contended that the scientific literature cited by Dr Cai contradicted his conclusion.

They also argued that Dr Tay did not cite any evidence to support his conclusion that cultural factors play such a role.

"It is absurd, irrational and discriminatory to criminalise a person on the basis of his natural, unchangeable identity and for non-harmful private acts," the team said in a statement to the media summarising their arguments.

The lawyers noted that their case differs from a previous case brought against Section 377A in 2010 by Mr Tan Eng Hong, whose lawyer had argued that there was overwhelming evidence that a person's sexual orientation is biologically determined.

Mr Tan had provided the court with statements from medical and scientific bodies which were not formally entered as evidence, they said.

"For the first time, there is expert evidence before the courts on the nature of sexual orientation. In the previous cases, the court was only asked to take judicial notice of scientific facts which required a different legal test," the lawyers said in their statement.

The first of the three recent cases, brought by Mr Bryan Choong Chee Hong, 42, the former executive director of lesbian, gay, bisexual and transgender (LGBT) non-profit Oogachaga, was heard last week.

The third case, brought by LGBT activist and retired general practitioner Tan Seng Kee, was also heard on Monday.

Mr M. Ravi of Carson Law Chambers, who represented Dr Tan, argued that other laws make it legally obligatory for anyone to report those who violate Section 377A, including gay men themselves, their friends or family members, and their medical care providers.

For example, Section 424 of the Criminal Procedure Code (CPC) states that every person aware of the commission of - or the intention of any other person to commit - any arrestable offence punishable under Chapter XVI of the Penal Code, among others, shall report that commission or intention to the police. Section 377A falls under Chapter XVI of the Penal Code.

Mr Ravi argued that Parliament's stance that Section 377A will not be proactively enforced "interferes with Article 9(1) of the Constitution, as it leads to an inconsistent and arbitrary application of criminal procedure as well as being incongruous with the mandatory obligation" under Section 424 of the CPC.

The three cases were heard by Justice See Kee Oon in chambers and were not open to the public.

The AGC began its submissions on Monday and will conclude by the end of the day or at the next hearing on Wednesday.

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Sexual orientation cannot be wilfully changed, say lawyers fighting to repeal Section 377A - The Straits Times

Researchers have found that taller people have an increased risk of developing atrial fibrillation (AFib), an irregular and often rapid heartbeat that can lead to stroke, heart failure and other complications.

The research, which reveals a strong link between the genetic variants associated with height and one's risk for AFib, is the among the first to demonstrate that height may be a causal--not correlated--risk factor for AFib.

Researchers found that the risk for AFib climbed as one's height increased, with every one-inch increase in height translating to about a three percent increase in risk of Afib--independent of other clinical factors--as compared to those at average height (5 feet and 7 inches).

"Our findings suggest it may be beneficial to incorporate height into risk-prediction tools for AFib," said the study's lead author Michael Levin from University of Pennsylvania.

"While current guidelines advise against widespread screening for AFib, our findings show that a certain group of patients--specifically, very tall patients--may benefit from screening," Levin added.

AFib, which affects more than 33 million people worldwide, is a common, abnormal heart rhythm.

There are a number of clinical risk factors for developing AFib, including high blood pressure, heart disease, diabetes, and obesity.

Observational studies, examining population-level data, have found that taller individuals appear to have a higher risk of developing AFib.

To further examine the association between height and Afib, the research team leveraged data from the Genetic Investigation of Anthropometric Trials (GIANT) consortium, which studied more than 700,000 individuals to identify genetic variants associated with height.

They also examined data from the Atrial Fibrillation Genetics (AFGen) consortium, which studied more than 500,000 individuals to identify genetic variants associated with AFib.

The authors employed a statistical method which uses genetics to precisely estimate the relationship between two traits.

Their analysis revealed that genetic variants associated with height were also strongly associated with Afib, suggesting that increased height may be a cause of atrial fibrillation.

This relationship remained strong even after adjusting for traditional AFib risk factors, like heart disease, high blood pressure, and diabetes, among others.

From there, researchers used a similar statistical method to conduct an individual-level analysis of nearly 7,000 individuals enrolled in the Penn Medicine Biobank.

They found that height, and genetic variants associated with height, are strongly associated with an increased risk of AFib, independent from traditional clinical and echocardiographic risk factors.

"These analyses show how we can use human genetics to help us better understand causal risk factors for common disease," said the study's senior author Scott Damrauer.

The study is scheduled to be presented at American Heart Association 2019 Scientific Sessions in Pennsylvania, US.

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Taller People have Increased Risk of Irregular Heartbeat - News18

A new study led by researchers at Baylor College of Medicine revealed how in utero Zika virus infection can lead to microcephaly in newborns. The team discovered that the Zika virus protein NS4A disrupts brain growth by hijacking a pathway that regulates the generation of new neurons. The findings point at the possibility of developing therapeutic strategies to prevent microcephaly linked to Zika virus infection. The study appeared Thursday in the journal Developmental Cell.

Patients with rare genetic mutations shed light on how Zika virus causes microcephaly

The current study was initiated when a patient presented with a small brain size at birth and severe abnormalities in brain structures at the Baylor Hopkins Center for Mendelian Genomics (CMG), a center directed by Dr. Jim Lupski, professor of pediatrics, molecular and human genetics at Baylor College of Medicine and attending physician at Texas Childrens Hospital, said Dr. Hugo J. Bellen, professor at Baylor, investigator at the Howard Hughes Medical Institute and Jan and Dan Duncan Neurological Research Institute at Texas Childrens Hospital.

This patient and others in a cohort at CMG had not been infected by Zika virus in utero. They had a genetic defect that caused microcephaly. CMG scientists determined that the ANKLE2 gene was associated with the condition. Interestingly, a few years back the Bellen lab had discovered in the fruit fly model that ANKLE2 gene was associated with neurodevelopmental disorders. Knowing that Zika virus infection in utero can cause microcephaly in newborns, the team explored the possibility that Zika virus was mediating its effects in the brain via ANKLE2.

In a subsequent fruit fly study, the researchers demonstrated that overexpression of Zika protein NS4A causes microcephaly in the flies by inhibiting the function of ANKLE2, a cell cycle regulator that acts by suppressing the activity of VRK1 protein.

Since very little is known about the role of ANKLE2 or VRK1 in brain development, Bellen and his colleagues applied a multidisciplinary approach to tease apart the exact mechanism underlying ANKLE2-associated microcephaly.

The fruit fly helps clarify the mystery

The team found that fruit fly larvae with mutations in ANKLE2 gene had small brains with dramatically fewer neuroblasts brain cell precursors and could not survive into adulthood. Experimental expression of the normal human version of ANKLE2 gene in mutant larvae restored all the defects, establishing the loss of Ankle2 function as the underlying cause.

To understand why ANKLE2 mutants have fewer neuroblasts and significantly smaller brains, we probed deeper into asymmetric cell divisions, a fundamental process that produces and maintains neuroblasts, also called neural stem cells, in the developing brains of flies and humans, said first author Dr. Nichole Link, postdoctoral associate in the Bellen lab.

Asymmetric cell division is an exquisitely regulated process by which neuroblasts produce two different cell types. One is a copy of the neuroblast and the other is a cell programmed to become a different type of cell, such as a neuron or glia.

Proper asymmetric distribution and division of these cells is crucial to normal brain development, as they need to generate a correct number of neurons, produce diverse neuronal lineages and replenish the pool of neuroblasts for further rounds of division.

When flies had reduced levels of Ankle2, key proteins, such as Par complex proteins and Miranda, were misplaced in the neuroblasts of Ankle2 larvae. Moreover, live imaging analysis of these neuroblasts showed many obvious signs of defective or incomplete cell divisions. These observations indicated that Ankle2 is a critical regulator of asymmetric cell divisions, said Link.

Further analyses revealed more details about how Ankle2 regulates asymmetric neuroblast division. They found that Ankle2 protein interacts with VRK1 kinases, and that Ankle2 mutants alter this interaction in ways that disrupt asymmetric cell division.

The Zika connection

Linking our findings to Zika virus-associated microcephaly, we found that expressing Zika virus protein NS4A in flies caused microcephaly by hijacking the Ankle2/VRK1 regulation of asymmetric neuroblast divisions. This offers an explanation to why the severe microcephaly observed in patients with defects in the ANKLE2 and VRK1 genes is strikingly similar to that of infants with in utero Zika virus infection, Link said.

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For decades, researchers have been unsuccessful in finding experimental evidence between defects in asymmetric cell divisions and microcephaly in vertebrate models. The current work makes a giant leap in that direction and provides strong evidence that links a single evolutionarily conserved Ankle2/VRK1 pathway as a regulator of asymmetric division of neuroblasts and microcephaly, Bellen said.

Moreover, it shows that irrespective of the nature of the initial triggering event, whether it is a Zika virus infection or congenital mutations, the microcephaly converges on the disruption of Ankle2 and VRK1, making them promising drug targets.

Another important takeaway from this work is that studying a rare disorder (which refers to those resulting from rare disease-causing variations in ANKLE2 or VRK1 genes) originally observed in a single patient can lead to valuable mechanistic insights and open up exciting therapeutic possibilities to solve common human genetic disorders and viral infections.

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How in utero Zika virus infection can lead to microcephaly in newborns: Baylor research - Outbreak News Today

By Stephanie Miceli | Nov. 13, 2019

When Sara Altschule took a 23andMe ancestry test, the results confirmed what she already suspected: She is 77 percent Ashkenazi Jewish. However, months later, after opting into add-on health tests, she received life-changing news: She had a BRCA2 gene mutation, which is particularly prevalent among Ashkenazi Jewish women. Altschules BRCA2 mutation meant her lifetime risk of developing breast cancer is about 69 percent; for ovarian cancer, it is about 17 percent.

As at-home genetic tests grow in popularity, some individuals have expressed concern about the complexities of the results. Speaking about her experience with at-home genetic testing at a recent workshop of the Roundtable on Genomics and Precision Health of the National Academies of Sciences, Engineering, and Medicine, Altschule told attendees, The results not only probably saved my life, but may have also saved the lives of people in my family who now know they are also BRCA2 positive. While empowering for her, she also wishes she had received the results from a genetic counselor not via email.

Traditionally, there have been two main types of genetic testing: traditional tests initiated by a doctor, and direct-to-consumer (at-home) tests. Most people do a combination of both, said keynote speaker Robert Nussbaum, chief medical officer of Invitae. About one-third of people who take an at-home test share the results with a provider, who can make appropriate referrals based on the results, he said.

Knowledge Is Power

After seeing a genetic counselor and getting a more comprehensive blood test, Altschule decided to undergo a preventive double mastectomy at the age of 31. I felt powerless during this process, and I wanted to take my power back. This was the easiest and toughest decision of my life, said Altschule.

Panelist Dorothy Pomerantz, who also received news of her BRCA status via 23andMe, said online test results are not a replacement for a one-to-one conversation with a trusted provider. Pomerantz considers herself lucky to have received actionable information, though she still has complicated feelings about how that information was delivered.

This information is complicated and nuanced. We need someone to walk us through the dark, said Pomerantz. When my genetic counselor confirmed my results, she asked me what I needed in that moment. Did I need to vent? Did I want information? Did I need to be alone or cry?

Affordability Is Part of Accessibility

Aside from having access to genetic testing in the first place, Altschule and Pomerantz acknowledged they had the resources to get immediate follow-up testing and surgery.

What about those who cant get their doctors on the phone? What about those who dont have doctors at all? asked Pomerantz.

Without insurance, someone with a risk of cancer may not have those options, said Sadie Hutson, director of the Cancer Genetics Program at Pikeville Medical Center in Kentucky. In the Appalachian communities where she works, coal mining, the dominant industry, has been linked to high incidences of lung cancer. However, many people have to live with the knowledge of that risk and the inability to act on it.

Affordability of genetic testing is a very real problem, said Hutson.

There is also a dire shortage of genetic counselors in the region, she added. Hutson has partnered with mobile clinics and faith-based organizations that provide genetic testing and counseling free of charge, particularly to the regions Medicaid population. Hutson also noted the importance of offering free follow-up testing to family members.

Panelists discussed the accessibility of direct-to-consumer genetic tests for underserved and rural populations and ways to increase engagement, literacy, and reduce disparities.

Steps Toward Including All of Us

We have a skewed evidence base in human genomics research, said Malia Fullerton, professor of bioethics and humanities at the University of Washington School of Medicine. Because certain populations are underrepresented in research, when they do receive genetic testing, there is a lack of data that they can act on. Joyce Tung, 23andMes vice president of research, acknowledged most of the companys customers are white people of European descent and it wants to change that.

We cant provide information that we dont have, she said. A lack of data can halt progress and new discoveries in diseases that primarily affect diverse communities such as sickle cell disease, which is prevalent in people of African descent. Tung highlighted several initiatives at 23andMe that aim to improve diversity, including the African American Sequencing Project, Global Genetics Project, and the Latino Sequencing Project.

In addition, underrepresented populations are more likely to receive uncertain test results, often because their genetic variants have not been well-studied. As a result, they may experience unnecessary testing or lifestyle changes, or false reassurance, and the psychological burden that comes with it, Fullerton said.

To address the lack of diversity in genetic databases, last year, the National Institutes of Health launched its All of Us research initiative. It aims to collect data from 1 million Americans from various population groups.

The vast majority of 23andMe consumers 80 percent agree to share their data in the hopes of contributing to science and new insights about health and disease. However, the current lack of diversity in genetic databases risks hindering the science.

There is a critical opportunity for multiple sectors to come together to ensure proper inclusion of all individuals in genetic and genomic testing, said Hutson.

Integrating Consumer Genomics into Health Care

Speakers throughout the day acknowledged the challenges around integrating consumer genomics data into clinical care. Consumers often want information fast, but health systems may not be able to quickly provide the confirmation genetic testing following a positive DTC result.

This continuum of care has a lot of access points and a lot of people trying to find pathways, but really it is reflective of the overall health system, said Siobhan Dolan, a professor and vice chair for research at Albert Einstein College of Medicine. Maybe genetics has given people an opportunity to find alternative routes and maybe we could continue to learn from that try to put something together that is continuous.

Visit http://nationalacademies.org/hmd/Activities/Research/GenomicBasedResearch/2019-OCT-29.aspx to view speaker presentations and other information about the Workshop on Exploring the Current Landscape of Consumer Genomics.

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At-Home DNA Tests Still Need the 'Human Touch,' Say Panelists at Genomics Roundtable Workshop - National Academies of Sciences, Engineering, and...

"It has a whole bunch of other things surrounding it, but it creates depressive symptoms."

According to SANE Australia, up to 4 per cent of Australians will develop BPD at some point in their life, with the symptoms usually manifesting in late adolescence.

Sufferers have trouble managing their emotions and impulses, and can also struggle to maintain a stable self-image.

The causes of BPD are not well understood, although they are believed to be a combination of biological and lifestyle factors.

Ms Collett said despite her diagnosis being relatively simple compared to other mental health issues, it was "frustrating" that there still wasnt a clear diagnosis and treatment for many sufferers.

Its hoped that new research from QIMR Berghofer Medical Research Institute could help change that, with scientists there identifying key areas on the human genome with direct links to depressive symptoms.

Senior study investigator Professor Eske Derks said the research uncovered seven distinct regions on the human genome with links to symptoms.

"We identified, for the first time, three genetic regions related to sleep problems, two for anhedonia [a loss of interest or pleasure in life], one related to changes in appetite, and one for depressed mood," Professor Derks said.

Overall, about one in 11 people, or 9 per cent of Australians, reported having depression or depressed feelings in 2014-15, according to figures from the Australian Bureau of Statistics.

The QIMR findings provide insight into why the symptoms of depression can vary hugely between patients, and they point the way to more targeted therapies.

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"In some patients, depression will manifest as a reduced appetite, while for others, there will be increased appetite," Professor Derks said.

"So normally if youre looking for the genetic risk factors for depression, you tend to collapse all of these symptoms together, even though they can be quite different from patient to patient."

Professor Derks said being able to accurately assess exactly what genes were in play for individual patients meant they would be able to get tailored treatment instead of the current method of "trial and error", where patients are prescribed the most common medication and then put on other drugs if that fails.

Ms Collett said it would be a comfort going forward to have a more certain diagnosis.

"Im naturally curious about my own health situation, so it would be really good to know the underlying reason why I have it. Was it genetics? Was it something that happened when I was a kid? Who knows?" she said.

The study, which examined genetic data and self-reported symptoms from 150,000 people from the UK Biobank, has been published in the journal Psychological Medicine.

Stuart Layt covers health, science and technology for the Brisbane Times. He was formerly the Queensland political reporter for AAP.

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Clear link between genetics and depressive symptoms uncovered - The Age

SOUTH SAN FRANCISCO, Calif., Nov. 12, 2019 (GLOBE NEWSWIRE) -- Alector, Inc. (Nasdaq: ALEC), a clinical stage biotechnology company pioneering immuno-neurology, today announced Company highlights and financial results for the third quarter of 2019.

We continue to integrate insight from human genetics, immunology, and neuroscience to advance our portfolio of novel therapeutics. AL001 has advanced to a Phase 2 trial in two genetically defined patient populations suffering from frontotemporal dementia. In addition, AL002 and AL003 are currently being evaluated in Phase 1b clinical trials in Alzheimers disease patients, said Arnon Rosenthal, Ph.D., Alectors chief executive officer. We are looking forward to our first presentation of data from the AL002 program taking place at the CTAD annual meeting and an update on our clinical and development pipelines at our R&D Day in December.

Recent Business Highlights

Third Quarter 2019 Financial Results

Revenue. Collaboration revenue for the third quarter of 2019 was $2.7 million compared to $6.5 million for the same period in 2018. Alector recognizes revenue from the upfront payments under the AbbVie Agreement over time as the services are provided. Revenues are recognized as the program costs are incurred by measuring actual costs incurred to date compared to the overall total expected costs to satisfy the performance obligation. Changes in estimates for revenue recognized over time are recognized on a cumulative basis.

R&D Expenses. Total research and development expenses for the third quarter of 2019 were $28.5 million compared to $20.4 million for the same period in 2018. The increase was driven by higher personnel-related expenses as headcount grew to support the advancement of the clinical and preclinical programs, increased expenditures related to the clinical trials, increased laboratory expenses for the development of our pipeline, and increased facilities and other unallocated research and development expenses to support the growth of the business.

G&A Expenses. Total general and administrative expenses for the third quarter of 2019 were $8.3 million compared to $2.9 million for the same period in 2018. This increase was primarily due to higher personnel-related expenses, increased facilities and general overhead expenses, and increased expenses related to information technology, accounting, legal, human resources, and other administrative functions to support the growth of the business.

Net Loss. For the third quarter of 2019, Alector reported a net loss of $31.7 million, compared to a net loss of $15.3 million for the same period in 2018.

Cash Position. Cash, cash equivalents, and marketable securities were $381.4 million as of September 30, 2019.

About AlectorAlector is a clinical stage biotechnology company pioneering immuno-neurology, a novel therapeutic approach for the treatment of neurodegenerative diseases. Immuno-neurology targets immune dysfunction as a root cause of multiple pathologies that are drivers of degenerative brain disorders. Alector is developing a broad portfolio of programs designed to functionally repair genetic mutations that cause dysfunction of the brains immune system and enable the rejuvenated immune cells to counteract emerging brain pathologies. The Companys product candidates are supported by biomarkers and target genetically defined patient populations in frontotemporal dementia and Alzheimers disease. Alector is headquartered in South San Francisco, California. For additional information, please visit http://www.alector.com.

Cautionary Note Regarding Forward-Looking Statements

This press release contains forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995. Such forward-looking statements are based on our beliefs and assumptions and on information currently available to us on the date of this press release. Forward-looking statements may involve known and unknown risks, uncertainties and other factors that may cause our actual results, performance or achievements to be materially different from those expressed or implied by the forward-looking statements. These statements include but are not limited to statements regarding the Companys financial condition and results of operations, and plans for the Companys product candidates, clinical studies and anticipated regulatory and development milestones. Except as required by law, we assume no obligation to update these forward-looking statements publicly, or to update the reasons actual results could differ materially from those anticipated in the forward-looking statements, even if new information becomes available in the future. Important factors that could cause our actual results to differ materially are detailed from time to time in the reports Alector files with the Securities and Exchange Commission, including in our quarterly report on Form 10-Q that is being filed with the Securities and Exchange Commission (SEC). Copies of reports filed with the SEC are posted on Alectors website and are available from Alector without charge.

Selected Consolidated Balance Sheet Data (in thousands)(unaudited)

(1) Upon the closing of our IPO in February 2019, all of the outstanding shares of our convertible preferred stock converted into 45,374,836 shares of common stock.

Consolidated Statement of Operations Data(in thousands, except share and per share data)(unaudited)

Source: Alector, Inc.

Contacts

Media:1ABDan Budwick, 973-271-6085dan@1abmedia.com

orInvestors:Alector, Inc.ir@alector.com

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Alector Reports Recent Business Highlights and Third Quarter 2019 Financial Results - GlobeNewswire

In a surprising finding using the standard animal model of Down syndrome (DS), scientists were able to correct the learning and memory deficits associated with the condition the leading genetic cause of cognitive disability and the most frequently diagnosed chromosomal disorder in the U.S. with drugs that target the bodys response to cellular stresses.

In a study published Nov. 14, 2019, in the journal Science, a team led by researchers at UC San Francisco and Baylor College of Medicine show that some of the intellectual impairments associated with DS may be traced to altered protein production in a region of the brain called the hippocampus, which is central to learning and long-term memory formation.

But in the so-called Ts65Dn mouse, engineered to capture genetic, behavioral and cognitive features of human Down syndrome, these changes can be undone. When the researchers administered drugs that target one of the cells key stress response pathways, they were able to bring protein levels back to normal, which caused the cognitive deficits typical of the Ts65Dn mouse to vanish.

Although the cognitive features of DS have generally been thought of as irreversible, the researchers say, these findings indicate that it may be possible to improve cognitive function in human DS using similar compounds.

Because DS is caused by an extra copy of chromosome 21, scientists have generally studied the disease through the lens of genetics, focusing primarily on ways in which the superfluous chromosome disrupts normal gene activity. But in the new study, rather than restricting their efforts to genes and chromosomes, the scientists trained their sights on the largely unexplored role of proteostasis a technical term for the cells protein manufacturing and quality control machinery in DS.

Peter Walter, Ph.D., co-senior author of the study, spearheaded the research to uncover a link between proteostasis defects and DS.

The vast majority of the field has been focusing on individual genes on chromosome 21 to figure out which ones are causally related to Down syndrome and its pathologies. Our approach was different. We were trying to uncover a link between proteostasis defects and DS, said Peter Walter, Ph.D., professor of Biochemistry and Biophysics at UCSF and co-senior author of the new study.

Walter spearheaded the new study with collaborator Mauro Costa-Mattioli, Ph.D., a professor of neuroscience at Baylor College of Medicine who is currently a visiting professor in Walters lab thanks to a UCSF Presidential Chair Award.

To identify proteostasis problems that might contribute to DS, the researchers turned to a common mouse model that captures most of the chromosomal, developmental and cognitive abnormalities that define the human version of the syndrome.

Using polysome profiling, a technique that allows scientists to take a detailed snapshot of the cells protein factories in action, the researchers found that up to 39 percent less protein was being produced in the hippocampus of DS mice, prompting them to ask why extra copies of genes could lead to a decline in protein production.

The researchers discovered that hippocampal cells in DS mice had activated whats known as the integrated stress response (ISR), a biological circuit that detects when somethings awry the presence of an extra chromosome, for example, in the case of DS and engages a protective response that activates machinery to tamp down protein production.

The cell is constantly monitoring its own health. When something goes wrong, the cell responds by making less protein, which is usually a sound response to cellular stress. But you need protein synthesis for higher cognitive functions, so when protein synthesis is reduced, you get a pathology of memory formation, said Walter.

Backing up these results, the scientists also found that the ISR was also activated in postmortem samples of brain tissue from people with DS. And by a stroke of pure luck, the researchers were able to obtain a tissue sample from a person with DS in whom some cells carried the expected third copy of chromosome 21, while others were genetically normal the ISR, however, was only active in the cells with the extra chromosome.

Taken together, these findings strongly suggest that the ISR is involved in, and perhaps even responsible for, certain DS symptoms.

Though the ISR can be activated by four different enzymes, the scientists found that only one of them, named PKR, was involved in activating the ISR in hippocampal cells in DS. By blocking the activity of PKR they were able to prevent ISR activation and reverse the declines in protein production that had been observed in the brains of DS mice. But even more impressive, the researchers found that blocking the ISR significantly improved cognitive function in these mice as well.

The researchers used three different approaches to dial down ISR activity deleting the PKR gene, using a drug that suppresses PKR activity, and finally, using a safe, well-studied drug called ISRIB that activates protein-manufacturing machinery that competes directly with the ISRs efforts to shut off protein production. All three approaches yielded a marked improvement in cognition, as demonstrated by two different memory and learning tests.

We started with a situation that looked hopeless, nobody thought anything could be done. But we may have struck gold.Peter Walter, Ph.D.

Importantly, these changes were physiological as well as behavioral. DS mice that were given ISR inhibitors showed improved function at synapses, sites between nerve cells where changes associated with learning take place. In fact, after ISR activity was blocked, the brains of DS mice were transmitting fewer of the inhibitory signals that can make it harder for the brain to learn and form new long-term memories.

Though the results of the study were extremely promising, Walter cautions that much more in this area remains to be studied. Still, the findings are an important first step toward finding therapies that could improve the lives and overall health of people living with DS, a condition that has generally been considered untreatable.

We started with a situation that looked hopeless, Walter said. Nobody thought anything could be done. But we may have struck gold.

Authors: Additional authors include Ping Jun Zhu, Sanjeev Khatiwada, Ya Cui, Lucas C. Reineke, Sean W. Dooling, Jean J. Kim, and Wei Li of the Baylor College of Medicine. Peter Walter is also a Howard Hughes Medical Institute investigator.

Funding: This study was funded by NIH grants R01NS076708, R01HG007538, R01CA193466 and R01 CA228140, Sammons Enterprises and the Howard Hughes Medical Institute.

Disclosures: Peter Walter is an inventor on U.S. Patent 9708247 held by the Regents of the University of California that describes ISRIB and its analogs. Rights to the invention have been licensed by UCSF to Calico LLC. Wei Li is a consultant for the Chosen Med. The authors declare no other competing interests.

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In Down syndrome mouse model, scientists reverse intellectual deficits with drugs - University of California

As the legendary science fiction author Arthur C Clarke once suggested, JBS Haldane was perhaps the most brilliant science popularizer of his generation. #LostTales

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JBS Haldane ranks among the greatest scientists of the 20th century, particularly for his invaluable contribution to our understanding of genetics. More fascinatingly, however, this remarkable polymath left his home country of the United Kingdom in 1957 and moved to India permanently. He took up residence and Indian citizenship with his wife Helen Spurway, a gifted biologist in her own right.

Never before in the 20th century had a scientist of his standing chosen to take his scientific research to India from the Westnot to mention becoming a citizen.

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Born on 5 November 1892, in Oxford, England, JBS grew up in privilege with his father John Scotee Haldane, an Oxford University physiologist. JBS was a child prodigy, learning how to read and acquiring a certain degree of familiarity with scientific terminology by the tender age of three. The influence of John Scott loomed large on his son with the duo acting as their own guinea pigs in various experiments, including ascertaining the physiological effects of poison gases.

But the turning point for JBS came when his father took him to a lecture by A D Darbishire, a British zoologist and geneticist, about legendary scientist Gregor Mendels laws of inheritance, dominance and segregation. The lecture facilitated his fascination with genetics.

JBS studied at Eton, an elite boys school, and subsequently at Oxford University, where he pursued the Classics and Mathematics, graduating with honours in 1914. However, his academic pursuits were brought to a halt by World War I. Commissioned to the British Army, he served in France and Iraq, where he was wounded.

Following the War, he came back to Oxford to pursue his research in genetics.

His most important genetical contributions were a series of mathematical papers on the effect of natural selection, which were summarized in his book, The Causes of Evolution. This work became the foundation for population genetics along with the works of R.A. Fisher and Sewall Wright. Haldane [also] introduced the important idea that immunity to infectious diseases played an important part in human evolutionHe emphasized the importance of ethical considerations in evaluating eugenic programs and the impact of in vitro fertilization, writes Krishna R Dronamraju, a colleague of JBS, for the Indian Journal of Human Genetics.

In many ways, JBS played a critical role in laying the foundation of classical human genetics.

He derived the law of steady-state kinetics in enzyme chemistry, besides ascertaining the physiological effects of carbon dioxide and carbon monoxide by testing them out on his own body, a method he learnt from his father.

After a four-year stint as a Professor of Genetics at the University College in London, he spent the next twenty as the Professor of Biometry. As a professed socialist and humanist, JBS was also deeply engaged in popularising the science to the masses beyond the laboratory.

As the legendary author Arthur C Clarke once suggested, JBS Haldane was perhaps the most brilliant science popularizer of his generation.

However, towards the fag end of his time in England, he grew increasingly disenchanted by British politics and society. The breaking point was his governments role in the Suez Crisis of 1956, which he saw as violations of international law, while admiring the Indian Independence Movement. Moreover, the warmer climate of India and Prime Minister Nehrus experiments with socialism also offered JBS and wife Helen with the necessary rationale for shifting base.

It was the legendary statistician P C Mahalanobis, who offered JBS a teaching position in the Indian Statistical Institute, Kolkata. At this time, he also began immersing himself in Indian philosophy and logic systems, applying indigenous knowledge systems to scientific research.

He continued his work in the study of genetics in India, ranging from studies about inbreeding in Andhra Pradesh, and colour blindness in Andhra and Odisha, apart from other such studies.

Never before in modern times had a Western scientist of Haldanes calibre chosen to move to India not to speak of becoming a citizen. He was critical of Indian science and scientists but saw hopes in young people. During his stay here, he did much for research in animal and human genetics and in support of science education, writes Dr Veena Rao, a faculty member at the National Institute of Advanced Sciences. Science, he believed, must help common citizens understand what goes on inside the research laboratories, for some of which he pays, writes Dr Veena Rao, Adjunct Faculty at the National Institute of Advanced Studies, for The Hindu.

He also criticised the bureaucratic roadblocks that stifled true research in India. There was even a dust-up between him and the management at the ISI, which led to his resignation and the eventual shift to Bhubaneswar, Odisha, on the invitation of Biju Patnaik.

Haldane was appointed [the] head of an entirely independent research establishment, where he worked with his young colleagues from Calcutta, including S D Jayakar, with whom he published papers on population genetics that are as enduring as the best of Haldanes early work, says this Down to Earth profile.

Whats particularly remarkable about his life is how quickly people forgot him. More than anything else, however, he passed on to his students and peers a passion for the sciences.

Also Read:This is Your Prize, Sir. How a Pak Nobel Laureate Paid Tribute to His Indian Guru

Just before passing away on 1 December 1964 of rectal carcinoma, he issued strict instructions that he wanted to dedicate his body to scientific researchthe mark of a true scientist.

Our only hope of understanding the universe is to look at it from as many different points of view as possibleNow, my own suspicion is that the universe is not only queerer than we suppose, but queerer than we can suppose, he wrote.

(Edited by Shruti Singhal)

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One of the World's Greatest Geneticists, He Gave Up British Citizenship for India - The Better India

The legal team advocating the repeal of Section 377A of the Penal Code which criminalises acts of gross indecency between men argued before the High Court on Mon (18 Nov) that sexual orientation is a product of genetic and environmental factors, and cannot be changed at will.

Lawyers Eugene Thuraisingam, Suang Wijaya and Johannes Hadi of Eugene Thuraisingam LLP, on behalf of applicant DJ Johnson Ong Ming, said that the preponderance of scientific evidence shows that human sexual orientation ranges along a continuum, from completely heterosexual to completely homosexual.

In between are bisexuals who have varying degrees of preference for either sex, the lawyers added.

Homosexuals, like heterosexuals, cannot wilfully change their sexual orientation and/or attraction. There is no credible scientific evidence which supports the proposition that therapy aimed at changing sexual orientation (such as reparative or conversion therapy) is safe or effective, they argued.

Consequently, the crux of the legal teams argument is that Section 377A in the Penal Code violates two provisions in the Singapore Constitution, namely Article 9 of the Constitution which guarantees the right to life and personal liberty, and Article 12 which guarantees equal protection before the law.

Sexual activity between consenting adult males in private, according to Mr Ongs lawyers, neither harms nor impinges upon the rights or interests of any other persons.

Section 377A therefore violates Article 9 and 12 of the Constitution. It is absurd, irrational and discriminatory to criminalise a person on the basis of his natural, unchangeable identity and for non-harmful private acts, they added.

The relevant section in the Penal Code also reinforces the majoritys good old-fashioned discrimination against male homosexuals, who are a minority in Singapore, according to Ongs legal team.

The role of our Constitution and the Court is to protect minorities against the absurd, irrational prejudices of the majority, his lawyers argued.

Three medical experts were called by Mr Ongs legal team in the immediate case, namely:

The Attorney-Generals Chambers (AGC), the respondent in all three cases, called the following experts:

Little to no scientific evidence in support of proposition pinpointing socio-environmental factors as cause for homosexuality and bisexuality, according to medical experts on both sides

Experts from both sides concurred that genetic and non-social environmental factors (like the womb environment) contribute to the causality of sexual orientation and/or attraction.

There is little if any scientific evidence which supports the proposition that social environmental factors (like culture, parenting) play any role in the causality of sexual orientation and/or attraction, said Mr Ongs lawyers.

One of the sources cited by Dr Cai is a study by Bailey, J.M., Vesey, P.L., Diamond, L.M., Breedlove, S.M., Villian, E,M & Epprecht, M. (in press), titled Sexual orientation controversy, and science, Psychological Science in the Public Interest, 2016, Vol 17(2) 45-101 summarises the position, which details the following:

No causal theory of sexual orientation has yet gained widespread support. The most scientifically plausible causal hypotheses are difficult to test. However, there is considerably more evidence supporting non-social causes of sexual orientation than social causes.

This evidence includes the cross-culturally robust finding that adult homosexuality is strongly related to childhood gender non-conformity; moderate genetic influences demonstrated in well sampled twin studies; the cross-culturally robust fraternal birth order effect on male sexual orientation; and the finding that when infant boys are surgically and socially changed into girls, their eventual sexual orientation is unchanged (i.e., they remain sexually attracted to females).

In contrast, evidence for the most commonly hypothesized social causes of homosexuality sexual recruitment by homosexual adults, patterns of disordered parenting, or the influence of homosexual parents is generally weak in magnitude and distorted by numerous confounding factors.

Citing Dr Cais report, the lawyers argued that it can be inferred that Dr Cais findings align with those of Dr Rajesh, who posited that biological and non-social environmental factors influence sexual orientation, and that [e]vidence for the most commonly hypothesised social causes of homosexuality have generally been debunked.

First, Dr Cai states that [s]exual orientation is no unchanging in everyone, and cites studies showing that some individuals have been found to experience spontaneous and naturally-occurring changes in sexual orientation, as opposed to willful changes.

Second, Dr Cai does not cite any literature or study supporting the proposition that sexual orientation can be willfully changed, such as through sexual orientation change efforts, conversion therapy or reparative therapy.

Mr Ongs lawyers also argued that Dr Cai has offered no credible evidence that sexual orientation can be willfully changed.

Studies showing that some individuals experience spontaneous and naturally occurring change in sexual orientation is nothing to the point, they argued, citing two reasons, namely:

i) spontaneous and naturally-occurring change is not willful change as demonstrated by the literature cited by Dr Cai himself; and

(ii) the studies show that close to 100% of homosexual males do not experience even any spontaneous or natural change.

Secondly, said Ongs lawyers, the literature cited by Dr Cai himself supports the point that persons do not experience choice over their sexual orientation and/or sexual attraction.

Ongs legal team added that the literature cited by Dr Cai demonstrates that there is no credible evidence for the purported effectiveness of conversion therapy, reparative therapy, and other forms of intervention to change sexual orientation are effective, which have been known present a significant risk of harm to individuals undergoing such interventions.

Genetics and other biological factors, including non-social environmental factors, contribute strongly to the development of sexual orientation

Another source cited by Dr Cai is a study by Roselli, C.E. titled Neurobiology of Gender Identity and Sexual Orientation, published in Journal of Neuroendocrinology, 2018, which states the following:

Most people experience little or no sense of choice about their sexual orientation. There Is no scientifically convincing research to show that therapy aimed at changing sexual orientation (ie, reparative or conversion therapy) is safe or effective. The origin of sexual orientation is far from being understood, although there is no proof that it is affected by social factors after birth. On the other hand, a large amount of empirical data suggests that genes and hormones are important regulators of sexual orientation

The data summarised in the present review suggest that both gender identity and sexual orientation are significantly influenced by events occurring during the early developmental period when the brain is differentiating under the influence of gonadal steroid hormones, genes and maternal factors. However, our current understanding of these factors is far from complete and the results are not always consistent

Our current understanding suffers from many limitations in the data Despite these limitations, the existing empirical evidence makes it clear that there is a significant biological contribution to the development of an individuals identity and sexual orientation.

Ongs lawyers pointed out thatDr Cai accepted the proposition that it is not disputed by experts in the field that genetics has some contribution to the causation of homosexuality.

Secondly, the lawyers highlighted that Dr Cai cited, in approval, papers which conclude that there can be little doubt that [sexual orientation] is influenced by environmental factors.

The environmental factors referred to by the papers cited by Dr Cai are non-social environmental factors such as the womb environment, not social environmental factors, Mr Ongs legal team highlighted, adding that Dr Cai has already cited various studies and literature pointing to genetic and non-social environmental factors of sexual orientation.

Dr Cai, according to the lawyers, also cited studies indicating that hormones play a part in the causation of sexual orientation, and the fraternal birth order effect play a role in shaping a persons sexual orientation.

Mr Ongs lawyers also rejected Dr Tays assertion that cultural and social environmental factors are also likely to play a role in determining sexual orientation, as the expert has cited no material that supports such an assertion.

This assertion is also demonstrably false, Mr Ongs lawyers argued.

The closed High Court hearing on Mon was the second out of three cases to be presented against Section 377A this month.

The current cases, according to a statement by Mr Ongs legal team, set a precedent in examining legal questions on the nature of sexual orientation, as expert evidence is now presented before the courts.

Previously, the court was only asked to take judicial notice of scientific facts which required a different legal test, Mr Ongs legal team added.

The AGC began its submissions on Mon, and will conclude its submissions at the next hearing on Wed.

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Section 377A constitutional challenge: Expert evidence reveal sexual orientation cannot be changed at will, lawyers argue - The Online Citizen

A University of California professor and co-originator of genome editing technology Clustered Regularly Interspaced Short Palindromic Repeats said researchers plan to expand the technology in order to increase human applications at a campus lecture series Thursday.

Jennifer Doudna, a UC Berkeley biochemistry professor, engaged students and the greater UCLA science community during the quarterly Donald J. Cram Distinguished Lecture series.

The Cram lecture series, a quarterly departmental event, invites prominent academics in the field of chemistry to speak about their research. The series is dedicated to Donald J. Cram, who was a Nobel laureate and a chemistry professor at UCLA for over 50 years.

This fall, the series was hosted by UCLA chemistry professor and Cram Chair Patrick Harran.

Scientists use CRISPR technology, formally known as CRISPR-Cas9, to modify DNA sequences and gene functions. Cas9 is a protein that can cut the strands of DNA-like molecular scissors.

CRISPR is studied and used by students, scientists and researchers to advance progress in the field of gene editing, in medicine and the life sciences.

The UC holds the largest CRISPR patent portfolio in the nation with 16 total patents, according to a UC Berkeley press release.

The United States Patent and Trademark Office granted the UC, along with the University of Vienna and Emmanuelle Charpentier, the director of the Max Planck Institute for Infection Biology, its 16th patent in October.

Doudnas involvement in CRISPR technology began around 2005, when a professor at UC Berkeley, Jill Banfield, invited Doudna to help her with research into the mechanism. From there, Doudna teamed up with Charpentier, who was working with a CRISPR system and its associated protein, Cas9, in 2011.

Doudna is one of the creators of the CRISPR utility for the permanent excision of harmful genes. Doudna said that she developed the idea for the CRISPR technology in 2011 in collaboration with Charpentier.

During the lecture, Doudna detailed how scientists regulate CRISPR enzymes to modify DNA.

CRISPR is a portion of the bacterial genomic sequence that acts as an adaptive immune system, Doudna said.

Bacteria encode the CRISPR system through viral infections, which allows its genome to recognize foreign DNA insertions. These DNA sequences incorporate themselves into the bacterial genome at the CRISPR locus, a genetic database of past infections.

Doudna said this locus was of unique interest to her.

Those sequences, called CRISPR, are transcribed in RNA molecules that provide the zip codes for Cas proteins, allowing them to recognize foreign DNA and cut it up, Doudna said.

Doudna and Charpentier, with the assistance of their team, were able to realize that CRISPR RNA is a 20-nucleotide sequence, which interacts with DNA in a complementary fashion.

This complementarity allows the protein to form a double-stranded break in DNA, necessitating a second RNA tracrRNA to form this functional unit, Doudna said.

And it was (biochemist) Martin Jinek in our lab who figured out that you could combine these two RNAs into a single guide RNA, Doudna said.

From this experiment, Jinek found that single guide RNAs were used by Cas9 to excise DNA at specific sites in a plasmid, a circular piece of bacterial DNA. The revelation from this was that, upon excision, DNA would repair itself in animals and plants, Doudna said.

Doudna said at the end of her talk that the system is becoming increasingly important in the field of medicine, and is currently being used at UCLA, by Donald Kohn, a professor of microbiology, immunology and molecular genetics.

Were within about five years, maybe less, from being able to make, essentially, any change to any genome in any type of cell, Doudna said.

Doudna stressed that this ability to make changes in the genome comes with bioethical responsibility for genome editing in humans.

Fourth-year biochemistry student Jeremy Shek, who attended the event, said although he had done a project that was an offshoot of CRISPR, he had not heard of the progress Doudna discussed.

It is important to be informed on advancements and progress in the field, he added.

Fourth-year bioengineering student Timothy Yu said he came to the lecture to see Doudna in person and get a more solid grasp on the methodology of CRISPR.

Lexi Omholt, a fourth-year microbiology, immunology and molecular genetics student, said that she came to the talk to understand the basis of CRISPR technology.

Jennifer Doudna was one of the reasons I chose my major, Omholt said. At that time, CRISPR came into popular knowledge, and the knockout tool was just coming into use. I am involved in a cancer lab, the Soragni Lab, that uses CRISPR-Cas9 on a regular basis.

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Co-creator of CRISPR lectures about future applications of genome editing technology - Daily Bruin