Cognitive Labs

"Chronometry led to the development of spreading activation models of memory wherein links in memory are not organized hierarchically but by 'relevance' instead."

--wikipedia


chronometry is the science of mental reaction time assessment

Cool site: stumbleupon.com
they picked up on the Cognitive Labs' research at Stanford/BrainAge/and our links to Dr. Ryuta 'learning therapy' Kawashima's work...

We hope to do some additional MRI in the near future. We've got an invite. Let's find out a) what your brain looks like taking cognitive labs tests b) eating blueberries or c) searching the web

let us know if you can think of anything else.

As promised, we are going to begin sharing some of the information we have collected on the physical and cognitive effects of spaceflight.

The following is available from NASA, other individuals who have been involved in conducting repeated physical exams on returning astronauts have discussed their data on physical changes: significant weight loss, loss of muscle mass, organ functioning changes, atrophy and lengthening of the extremities: it would be interesting to follow changes that occur once there is a semi-permanent base in space and individuals are effected for more than 1 year...and what, if any would be the effect on a second generation that was conceived and carried to gestation in space.

Current research on amphibians shows that upon return, space-born amphibians appear to be genetically encoded for the earth environment and return to 'normal' swimming behavior, but who knows how strong the encoding is and for what duration.

The site that you are helping with had around 32,000 page views yesterday, one of our top days: right about 1 million/month...

By stimulating a receptor in the brain that controls insulin responses, scientists have been able to halt or diminish the neurodegeneration of Alzheimer's disease. The finding provides possible evidence that the disease can be treated in its early stages, according to researchers at Rhode Island Hospital and Brown Medical School.

The activated receptor or agonist appears to block further abnormal cellular oxidation and accumulation of amyloid tangles.

Researchers have found that peroxisome-proliferator activated receptor (PPAR) agonists prevent several components of neurodegeneration and preserve learning and memory in rats with induced Alzheimer's disease (AD). They found that an agonist for PPAR delta, a receptor that is abundant in the brain, had the most overall benefit.

"This raises the possibility that you can treat patients with mild cognitive impairment who have possible or probable Alzheimer's disease. This is really amazing because right now, there's just no treatment that works," says lead author Suzanne M. de la Monte, MD, MPH, a neuropathologist at Rhode Island Hospital and a professor of pathology and clinical neuroscience at Brown Medical School in Providence, RI.

The study appears in the September issue (Volume 10, Issue 1) of the Journal of Alzheimer's Disease (http://www.j-alz.com).

In previous studies, the researchers demonstrated that Alzheimer's is a brain-specific neuroendocrine disorder, or a Type 3 diabetes, distinct from other types of diabetes. They showed that insulin and IGF-I receptors are produced separately in the brain, and begin to disappear early in Alzheimer's and continue to decline as the disease progresses. As insulin signaling breaks down, it leads to increased oxidative stress, impaired metabolism and cell death -- all causing neurodegeneration.

Scientists were also previously able to replicate Alzheimer's in rats with Streptozotocin (STZ), a compound that is known to destroy insulin producing cells in the pancreas and cause diabetes. When injected into the brains of rats, the compound mimicked the neurodegeneration of Alzheimer's disease -- plaque deposits, neurofibrillary tangles, diminished brain size, impaired cognitive function, cell loss and overall brain deterioration.