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Published on Jul 16, 2012

By Kezia Toh

More:
New dean for NTU's Lee Kong Chian School of Medicine

Photo by David W. Johnson, courtesy of the Alzheimers Association

Dr. Bradley T. Hyman, director of the Massachusetts Alzheimers Disease Research Center at Massachusetts General Hospital and a professor of neurology at Harvard Medical School, received the Henry Wisniewski Lifetime Achievement Award Sunday from Kristine Yaffe, a University of California, San Francisco professor at the Alzheimers Association International Conference in Vancouver, Canada.

By Gal Tziperman Lotan, Globe Correspondent

A Massachusetts General Hospital and Harvard Medical School neurologist received a lifetime achievement award at an Alzheimers Association conference in Vancouver, Canada Sunday.

Dr. Bradley T. Hyman, director of the Massachusetts Alzheimers Disease Research Center at Massachusetts General Hospital and a professor of neurology at Harvard Medical School, received the Henry Wisniewski Lifetime Achievement Award, The Alzheimer's Association said in a statement.

Its an extremely nice recognition, especially because the award is named after one of the giants of neuropathology, Hyman said in a phone interview from Vancouver Sunday.

Hyman has studied changes in patients brains and nervous systems, as well as genetic changes that underlie dementia, the statement said.

His research helps describe brain lesions in Alzheimer's patients, the statement said.

Hyman recently worked on imaging amyloid protein fragments that are broken down in healthy brains but accumulate and form amyloid plaques in Alzheimer's patients; and tau tangles, created when tau proteins that keep the brains cell transport system in working order die and collapse the system.

At its international conference, the Alzheimers Association also gave a lifetime achievement award to Lennart Mucke of the Gladstone Institute of Neurological Disease and the University of California, San Francisco, Monique M.B. Breteler of the German Center for Neurodegenerative Diseases and the University of Bonn in Germany, and Ronald Petersen of the Mayo Alzheimers Disease Research Center in Rochester, Minn.

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Harvard Medical School, MGH researcher honored for Alzheimer’s studies

Public release date: 15-Jul-2012 [ | E-mail | Share ]

Contact: Jim Fessenden james.fessenden@umassmed.edu 508-856-2000 University of Massachusetts Medical School

WORCESTER, Mass. A new genetic mutation that causes familial amyotrophic lateral sclerosis (ALS), a fatal neurological disorder also known as Lou Gehrig's Disease, has been identified by a team of scientists led by researchers at the University of Massachusetts Medical School (UMMS). Mutations to the profilin (PFN1) gene, which is essential to the growth and development of nerve cell axons, is estimated to account for one to two percent of inherited ALS cases. The finding, described today in the online edition of Nature, points to defects in a neuron's cytoskeleton structure as a potential common feature among diverse ALS genes.

"This discovery identifies what may possibly be a common biological mechanism involved across familial ALS cases regardless of genetics," said John Landers, PhD, associate professor of neurology and senior author of the study. "We know of at least three other ALS genes, in addition to PFN1, that adversely impact axon growth. If indeed, this is part of the disease's mechanism, then it might also be a potential target for therapeutics."

Robert Brown, MD, DPhil, a co-author on the study and chair of neurology at UMass Medical School, said "Dr. Landers has done great work in defining this new pathway for motor neuron death. We are delighted to have identified the defects in families from the U.S., Israel and France that we have been investigating for several years. Our finding is particularly exciting because it may provide new insights into ALS treatment targets."

ALS is a progressive, neurodegenerative disorder affecting the motor neurons in the central nervous system. As motor neurons die, the brain's ability to send signals to the body's muscles is compromised. This leads to loss of voluntary muscle movement, paralysis and eventually respiratory failure. The cause of most cases of ALS is not known. Approximately 10 percent of cases are inherited. Though investigators at UMass Medical School and elsewhere have identified several genes shown to cause inherited or familial ALS, almost 50 percent of these cases have an unknown genetic cause.

The current Nature study details the discovery of the PFN1 gene mutation among two large ALS families. Both families were negative for known ALS-causing mutations and displayed familial relationships that suggested a dominant inheritance mode for the disease. For each family, two affected members with maximum genetic distance were selected for deep DNA sequencing. To identify an ALS-causing mutation, genetic variations between the family members were identified and screened against known databases of human genetic variation, such as the 1000 Genomes Project. This narrowed down the resulting number of candidate, ALS-causing mutations to two within the first family and three within the second. Interestingly, both families contained different mutations within the same gene PFN1, the likely causative mutation. With additional screening, the team documented that in a total of 274 families sequenced, seven contained a mutation to the PFN1 gene, establishing it as a likely cause for ALS.

While it is not certain how the PFN1 mutation causes ALS, the cellular functions it controls within the motor neurons are responsible for regulation of a number of activities, including the growth and development of the axon, the slender projection through which neurons transmit electrical impulses to neighboring cells, such as muscle. When introduced into motor neuron cells, normal PFN1 protein was found diffused throughout the cytoplasm. Conversely, the mutant PFN1 observed in ALS patients was found to collect in dense aggregates, keeping it from functioning properly. Motor neurons producing mutated PFN1 showed markedly shorter axon outgrowth.

"The discovery that mutant PFN1 interferes with axon outgrowth was very exciting to us," said Claudia Fallini, PhD, a postdoctoral researcher at Emory University School of Medicine who collaborated with the UMass Medical School authors to investigate PFN1's functions in cultured motor neurons. "It suggests that alterations in actin dynamics may be an important mechanism at the basis of motor neuron degeneration."

"In healthy neurons, PFN1 acts almost like a railroad tie for fibrous filaments called actin, which make up the axon" said Landers. "PFN1 helps bind these filaments to each other, promoting outgrowth of the axon. Without properly functioning PFN1 these filaments can't come together. Here we show that mutant PFN1 may contribute to ALS pathogeneses by accumulating in these aggregates and altering the actin dynamics in a way that inhibits axon outgrowth."

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UMMS researchers isolate gene mutations in patients with inherited amyotrophic lateral sclerosis

An Uzbek man who pleaded guilty to plotting to assassinate President Barack Obama was never admitted to Columbia University's medical school, the university said Saturday, contrary to defense claims before he was sentenced to more than 15 years in prison.

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Columbia Univ.: Would-be assassin never admitted