In recent years researchers have demonstrated a number of ways to improve memory in old laboratory mice. Here is another:

If you forget where you put your car keys and you can't seem to remember things as well as you used to, the problem may well be with the GluN2B subunits in your NMDA receptors. And don't be surprised if by tomorrow you can't remember the name of those darned subunits. They help you remember things, but you've been losing them almost since the day you were born, and it's only going to get worse. An old adult may have only half as many of them as a younger person.

Cognitive decline with age is a natural part of life, and scientists are tracking the problem down to highly specific components of the brain. Separate from some more serious problems like dementia and Alzheimer's disease, virtually everyone loses memory-making and cognitive abilities as they age. The process is well under way by the age of 40 and picks up speed after that. But of considerable interest: It may not have to be that way. "These are biological processes, and once we fully understand what is going on, we may be able to slow or prevent it."

In recent research [scientists] used a genetic therapy in laboratory mice, in which a virus helped carry complementary DNA into appropriate cells and restored some GluN2B subunits. Tests showed that it helped mice improve their memory and cognitive ability. The NMDA receptor has been known of for decades. [It] plays a role in memory and learning but isn't active all the time - it takes a fairly strong stimulus of some type to turn it on and allow you to remember something. The routine of getting dressed in the morning is ignored and quickly lost to the fog of time, but the day you had an auto accident earns a permanent etching in your memory.

Within the NMDA receptor are various subunits, [and] research keeps pointing back to the GluN2B subunit as one of the most important. Infants and children have lots of them, and as a result are like a sponge in soaking up memories and learning new things. But they gradually dwindle in number with age, and it also appears the ones that are left work less efficiently. "The one thing that does seem fairly clear is that cognitive decline is not inevitable. It's biological, we're finding out why it happens, and it appears there are ways we might be able to slow or stop it, perhaps repair the NMDA receptors. If we can determine how to do that without harm, we will."

Link: http://oregonstate.edu/ua/ncs/archives/2013/aug/cognitive-decline-age-normal-routine-%E2%80%93-not-inevitable

Source:
https://www.fightaging.org/archives/2013/08/another-way-to-improve-memory-in-old-mice.php

Mitochondria are the power plants of the cell, generating chemical fuel stores that can be used to power cellular processes. They are important in aging, and this has a lot to do with the generation of reactive oxygen species (ROS) that happens as a side-effect of their operation. Researchers have shown that benefits to health and longevity can be realized in laboratory animals by targeting antioxidants to mitochondria in order to soak up some ROS before they cause harm. Other research focuses on repairing the damage that mitochondria inflict upon themselves this way, so as to stop it from contributing to degenerative aging.

There is general agreement that mitochondria play an important role in the aging process, but the role of mitochondrial oxidative stress remains controversial. Most previous work looking at mitochondrial oxidative stress has focused on damage to DNA, proteins, and lipids with age or in response to manipulation of cellular antioxidants. The interaction between oxidative damage and aging has been called into question in recent years by studies demonstrating little effect on aging and lifespan in mice with genetically modified antioxidant systems. A notable exception is the life extension and protection against multiple diseases in mice that express catalase in the mitochondria, which suggests that the cellular location and type of reactive oxygen species is an important factor.

Our laboratory is interested in whether redox inhibition of mitochondrial function contributes to age-related energy deficits in vivo in mouse and human skeletal muscle. [We] tested this hypothesis using a mitochondrial targeted peptide, SS-31, known to reduce mitochondrial H2O2 production.

SS-31 reduced the high mitochondrial H2O2 production from aged permeabilized muscle fibers [but] had no effect on young fibers. In the aged mice, one hour after in vivo treatment with SS-31 the cellular redox status [was] more reduced. This was accompanied by improved mitochondrial [function] in vivo in the skeletal muscle, while there was no effect on the mitochondrial energetics in young skeletal muscle. In addition to the improvements in muscle energetics, one hour and one week of SS-31 treatment resulted in improved muscle performance and increased exercise tolerance, respectively, in the old mice.

This rapid reversal of in vivo energy deficits supports the hypothesis that mitochondrial deficits in aged skeletal muscle are, at least in part, due to reversible redox sensitive inhibition. Thus assessing the role of mitochondrial oxidative stress in aging and disease will require careful attention to changes to the in vivo redox environment and the mechanisms by which these changes can affect cell function.

Link: http://impactaging.com/papers/v5/n8/full/100590.html

Source:
https://www.fightaging.org/archives/2013/08/targeting-redox-biology-to-reverse-mitochondrial-dysfunction.php