There was a time when I could hide my gray hairs with some strategic combing. Now, I have succumbed and describe my new hair color as “executive blond.” Of course, that also means that the important stuff under my scalp is getting older too. Brains start to “go gray” about the same time the hair does, which is why exercise for older adults has become the new anti-aging fix for our senior cerebellums. Several new studies provide more evidence that a brain in motion tends to remain... young.
A new study in Cell shows that Wnt signaling, already known to control many biological processes, between hair follicles and melanocyte stem cells can dictate hair pigmentation.

Using genetic mouse models, researchers were able to examine how Wnt signaling pathways enabled both hair follicle stem cells and melanocyte stem cells to work together to generate hair growth and produce hair color.

Research also showed the depletion (or inhibition or abnormal) Wnt signaling in hair follicle stem cells not only inhibits hair re-growth but also prevents melanocytes stem cell activation required for producing hair color. The lack of Wnt activation in melanocyte stem cells leads to depigmented or gray hair.
A new study offers insights about the interaction between a toxic protein called progerin and telomeres, which cap the ends of chromosomes like aglets, the plastic tips that bind the ends of shoelaces.   

Telomeres wear away during cell division. When they degrade sufficiently, the cell stops dividing and dies. The researchers have found that short or dysfunctional telomeres activate production of progerin, which is associated with age-related cell damage. As the telomeres shorten, the cell produces more progerin.

Progerin is a mutated version of a normal cellular protein called lamin A, which is encoded by the normal LMNA gene. Lamin A helps to maintain the normal structure of a cell's nucleus, the cellular repository of genetic information.
Okay, it's not really fair to call it a scam, but I just couldn't resist the alliteration. Here's what they say:
Squid skin is normally thrown away, but the Fisheries Research Institute [of Taiwan] announced recently that it has found a way to use it to produce functional peptides that can be sold as health care products or supplements . . . [The peptides] showed positive effects in slowing down the aging process and easing blood pressure . . . the peptides had not only proved safe but also activated neuron cells to help improve learning and reduce memory loss associated with aging.
A gene in the nucleus of muscle and brain cells named  MLIP (Muscle enriched A-type Lamin Interacting Protein) affects heart development and the aging process, according to a study in the Journal of Biological Chemistry .

Mutations in the Lamin gene family are associated with muscular dystrophy and other degenerative heart muscle diseases.    
“You have to bump the cage harder. Like this.”

Marta Santos took the plastic cage from my hands and smacked it with the palm of her hand, causing a few lifeless bodies to fall off the walls of the cube and collect on the floor. It was like kicking a vending machine so that the Snickers bar would drop into the compartment below. I took the cage back and, following suit, smacked it a few times, then watched the living fruit flies, or Drosophila melanogaster, whiz frantically around the confines of their plastic home, disturbed. I used a paintbrush to collect the dead and place them into a small plastic cap on the floor of the cage. They had, by experimental design, starved to death.
Up to 12 percent of Americans may get Alzheimer's disease, current statistics say.  In the quest to prevent Alzheimer's, or at least make it manageable like diabetes, a group of researchers are working on a nasally-delivered vaccine that promises to protect against Alzheimer's.  Bonus: It may help prevent strokes also.

The new vaccine repairs vascular damage in the brain by using the body's own immune system and, in addition to its prophylactic effect, it can work even when Alzheimer's symptoms are already present, according to the paper in Neurobiology of Aging.
Patients with Hutchinson-Gilford Progeria Syndrome age eight to 10 times faster than the rest of us and rarely live beyond 13 years. Almost all of the patients die from complications of arteriosclerosis, the clogging or hardening of arteries or blood vessels caused by plaques, which leads to heart attack and stroke.

Research on Progeria is difficult because the disease is exceedingly rare and only 64 children living with progeria are known, making access to patients very difficult.
When you were young you may have heard something about a dog like, "Fido is 10 years old, that is 70 in people years" and wondered what that meant.

It's a rule of thumb but there is a science basis to it, yet current methods of comparing patterns of aging are limited because they confound two different elements of aging – pace and shape.   And it can be confusing for non-biologists.
While the average lifespan of those who reach adulthood has continued to rise those years spent living without health issues have not kept pace.

From 1970 to 2005, the probability of a 65-year-old surviving to age 85 doubled, from about a 20 percent chance to a 40 percent chance and the presumption was that the same changes allowing people to live longer, including medical advances, would delay the onset of disease and allow people to spend fewer years of their lives with debilitating illness.

Instead, a 20-year-old today can expect to live one less healthy year over his or her life span than a 20-year-old a decade ago.

What gives?