Published on January 30th, 2013 | by Michael Ricciardi0
Science of Aging News: ‘Super Agers’ With More Brain Matter, Over-Fed Mitochondria, and a Molecule Reverses Memory Loss
The following is a roundup of some of the most notable, recent advances and discoveries in Aging research.
Like the body’s muscles, our brain matter shrinks as we age. Brain lobes become skinnier. Neurons “die off”. An average person at 80 has significantly less brain matter that an average person at 60. This diminishing of brain matter in turn leads to the cognitive decline scientists expect to see in those of more advanced age.
‘Super Agers’ have brains that resemble those of much younger people
But researchers at Northwestern University Feinberg School of Medicine have identified a group of octogenarians whose average brain thickness matched that of much younger persons (those aged 50 – 65 years) and who performed as well on memory tests as the younger group did.
Significantly, this group — called ‘super agers’ by the brain researchers — actually had thicker brain matter in a region called the anterior cingulate which is important for attention.
According to neuroscientist and lead researcher Emily Rogalski, it is probably this extra attention capability in super agers that serves to support their memory, but she notes that “there may be more than one way to becoming a Super Ager.”
That’s potentially good news for short attention span folks.
Importantly, comparisons with normal octogenarians using fMRI scans revealed that these super agers had on average four times more of a special class of cingulate neurons — called von Economo neurons — that are related to “higher order” thinking.
The research was published in the Journal of the International Neuropsychological Society.
Read more about this research in the Scientific American article.
Ageing and Mitochondrial “Over Eating”
For at least a decade or so, it has been theorized that the process of aging is due somehow to the “breakdown” of cellular mitochondria– the “power plants” of our cells. But just how this break down occurred, and what could cause it, has remained a biological mystery.
Now, biologists Daniel Gottschling and Adam Hughes at the Fred Hutchinson Cancer Research Center in Seattle, working with yeast cultures, have found compelling evidence that this mitochondrial break down is the result of a nutrient storage breakdown in another cell organelle (component) known as the vacuole.
A similar process occurs in some human cells, such as brains cells and pancreatic cells, and these are in turn associated with human diseases. In human cells, this vacuole is called the lysosome.
The main job of the vacuole (or lysosome) is twofold: to split up proteins (for later reuse) and to store nutrients that other cell organelles (like mitochondria) need. However, if the vacuole’s interior becomes too basic (too high pH) it’s ability to store nutrients properly is compromised and it releases nutrients into the cell interior (the cytoplasm)
Many of these excess nutrients are then taken up by the mitochondria causing a type of metabolic “burn out”, leading to deformed (“chunky”) and dysfunctional mitochondria…and eventually, age-related disease.
Researchers are calling the discovery “surprising” as they had not suspected that such a basic cellular component and function (storage) could, under high pH conditions, malfunction and lead to mitochondrial breakdown and aging.
The discovery led Hughes and Gottschling to commence new research on the effects of calorie restriction on the acidity of the vacuole. Although there have been some recent challenges to earlier findings, many studies have shown that caloric restriction extends lifespan. Experiments with yeast, worms, fruit flies and even some mammals seem to confirm the connection.
The researchers found that calorie restriction — reducing the supply of “raw materials” that the cell needs — did indeed lower the vacuole’s pH (making it more acidic) and delayed cell aging.
“Now that we have preliminary evidence in yeast of how calorie restriction extends lifespan, our hope is that it can be translated to higher organisms like humans,” Hughes said.[source, see article link below]
The next step for the researchers is to uncover the direct cause of the vacuole’s loss of acidity.
Read more about this key research in this World Science report.
Of Mice, Molecules and Memory
Researchers at the National Institute of Neurological Disorders and Stroke in Bethesda, Md., have found that a special molecule, called TFP5, when given to mice having a bio-engineered version of Alzheimer’s disease, repaired abnormal brain formations — the brain plaques and tangles typical of the disease — and thereby reversed memory loss.
As is often the case in biomedicine: it takes a molecule to block a molecule.
The experimental molecule was derived from another molecule that regulates the activity of a signaling molecule — an enzyme called Cdk5 * — whose over-signalling has been connected to the growth of the plaques and tangles found in the brain disease.
A healthy cell must maintain continuous control of a myriad of complex chemical processes. Cell organelles (components within the cell) must be able to communicate with each other, and transmit signals. To accomplish this, the cell utilizes a great many signaling pathways.
These pathways are mediated by a variety of molecules, may of which are types of enzymes called kinases (Cdk5 is a type of kinase). Over 500 types of kinases have been identified in the human body. Maintaining these signalling pathways is crucial for normal cellular functions. But as we age, our cells’ normal signalling can go awry and cause disease.
According to a press statement, the TFP5-treated mice showed “substantial reduction in the various disease symptoms along with restoration of memory loss.” [source: see link, below]
Further: the mice “experienced no weight loss, neurological stress (anxiety) or signs of toxicity.” And, importantly, the TFP5 mice lived on average two months longer than the control mice — which is the equivalent of five years in humans.
Of course the next step is to determine if this molecule — or a derivative one — works in humans as well as mice. If so, it could be one of the most promising advances in Alzheimer’s treatment to come along..
Perhaps the most devastating of age-related diseases, Alzheimer’s disease typically leads to severe memory loss and is nearly always fatal. Alzheimer’s currently affects 5 million Americans; almost half the U.S. population over 85 has Alzheimer’s.
* Cdk5 is involved in the processes of neuronal maturation, plasticity and migration
The findings are published in the January 2 issue of FASEB Journal, a medical research publication.
For more on this promising research, check out this World Science article
Top image: (The Fountain of Youth by Lucas Cranach the Elder
Second image: (Anterior cingulate gyrus of left cerebral hemisphere) ; Was a bee CC-By-SA 2.0
Third image: (dyed) Yeast cells (Courtesy of Gottschling Lab, Hutchinson Cancer Research Ctr.) via this World Science report