Tuesday, March 27, 2012

Chronic stress may lead to Alzheimer’s

Chronic stress may lead to Alzheimer’s: Repeated stress may trigger the production and accumulation of insoluble protein aggregates that are associated with Alzheimer’s, a new study has suggested.

The aggregates are similar to neurofibrillary tangles or NFTs, modified protein structures that are one of the physiological hallmarks of Alzheimer’s disease.

Friday, March 23, 2012

Brain insulin resistance contributes to cognitive decline in Alzheimer's disease

Brain insulin resistance contributes to cognitive decline in Alzheimer's disease: Insulin resistance in the brain precedes and contributes to cognitive decline above and beyond other known causes of Alzheimer's disease, according to a new study by researchers from the Perelman School of Medicine at the University of Pennsylvania. Insulin is an important hormone in many bodily functions, including the health of brain cells. The team identified extensive abnormalities in the activity of two major signaling pathways for insulin and insulin-like growth factor in non-diabetic people with Alzheimer's disease. These pathways could be targeted with new or existing medicines to potentially help resensitize the brain to insulin and possibly slow down or even improve cognitive decline.

New hope for treating Alzheimer's Disease: A role for the FKBP52 protein | Science Codex

New hope for treating Alzheimer's Disease: A role for the FKBP52 protein | Science Codex: New research in humans published today reveals that the so-called FKBP52 protein may prevent the Tau protein from turning pathogenic. This may prove significant for the development of new Alzheimer's drugs and for detecting the disease before the onset of clinical symptoms.A study published online today in the Journal of Alzheimer's Disease (1), for the first time demonstrates that the FKBP52 protein, discovered by Prof. Etienne BAULIEU twenty years ago, may prevent hyperphosphorylation of Tau protein, which has been shown to characterise a number of cerebral neurodegenerative diseases, including Alzheimer's Disease (AD).

Monday, March 19, 2012

Medical Report: Potential Alzheimer's Breakthrough | ABC 6 WJBF-TV

Medical Report: Potential Alzheimer's Breakthrough | ABC 6 WJBF-TV: It's long been the holy grail for doctors treating Alzheimer's: find a way to stop the rapid mental decline that is the hallmark of this debilitating disease.
Now a new clinical trial could just prove that possible, using a novel approach that could awaken memory circuits in the brain.
It's called Deep Brain Stimulation and it has already shown promise in a few Canadian patients with early Alzheimer's.
Four years ago Robert Linton had 2 electrodes implanted in the memory area of the brain. Every day since, a battery implanted in his chest has sent his brain more than 100 electrical impulses a second.

Thursday, March 8, 2012

Vitamin D may help treat Alzheimer's disease

Vitamin D may help treat Alzheimer's disease: Scientists have identified the intracellular mechanisms regulated by vitamin D3 that may help the body clear the brain of amyloid beta, the main component of plaques associated with Alzheimer's disease.

The findings revealed that vitamin D3 may activate key genes and cellular signalling networks to help stimulate the immune system to clear the amyloid-beta protein.

Previous laboratory work by the team demonstrated that specific types of immune cells in Alzheimer's patients might respond to therapy with vitamin D3 and curcumin, a chemical found in turmeric spice, by stimulating the innate immune system to clear amyloid beta. But the researchers didn't know how it worked.

Thursday, March 1, 2012

Scientists Show How to Remove Gene Blockade and Boost Cognition in Alzheimer Disease

GEN News Highlights:Scientists Show How to Remove Gene Blockade and Boost Cognition in Alzheimer Disease: Scientists say histone deacetylase 2 (HDAC2)-selective inhibitors may represent a therapeutic approach to slowing cognitive decline in patients with neurodegenerative disorders such as Alzheimer disease (AD). Researchers at the Massachusetts Institute of Technology’s (MIT) Picower Institute for Learning and Memory and Howard Hughes Medical Institute found increased levels of HDAC2 in two mouse models of AD and in human AD patients. These increased levels of the deacetylating enzyme were associated with the reductions in histone acetylation and expression levels of key learning-related genes.

Reversing Alzheimer’s gene ‘blockade’ can restore memory, other cognitive functions - MIT News Office

Reversing Alzheimer’s gene ‘blockade’ can restore memory, other cognitive functions - MIT News Office: MIT neuroscientists have shown that an enzyme overproduced in the brains of Alzheimer’s patients creates a blockade that shuts off genes necessary to form new memories. Furthermore, by inhibiting that enzyme in mice, the researchers were able to reverse Alzheimer’s symptoms.