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Although research has so far been confined to mouse studies, researchers are optimistic about the promise of histone deacetylase inhibitors in reversing age-related memory loss — both normal decline, and the far more dramatic loss produced by Alzheimer’s.
A comprehensive study reveals how the ‘Alzheimer's gene’ (APOE ε4) affects the nature of the disease. It is not simply that those with the gene variant tend to be more impaired (in terms of both memory loss and brain damage) than those without.
A few months ago, I reported on an exciting finding that rapamycin, a drug currently used in transplant patients, improved memory in Alzheimer's mice.
While everyone agrees that amyloid-beta protein is part of the problem, not everyone agrees that amyloid plaques are the cause (or one of them) of Alzheimer’s. Other forms of amyloid-beta have been pointed to, including floating clumps called oligomers or ADDLs.
Previous research has found that unexplained weight loss is an early sign of Alzheimer's.
The Phase II clinical trial of a treatment using naturally occurring antibodies (IGIV) has achieved significantly lower rates of ventricular enlargement (6.7% vs 12.7% per year) and less whole-brain atrophy (1.6% vs 2.2% per year) than control subjects who initially received placebo.
Another gene has been identified that appears to increase risk of Alzheimer’s. The gene, MTHFD1L, is located on chromosome six.
The American Academy of Neurology has updated its guidelines on when people with dementia should stop driving.
A brain scanning study using Pittsburgh Compound B, involving 42 healthy individuals (aged 50-80), of whom 14 had mothers who developed Alzheimer's, 14 had fathers with Alzheimer's, and 14 had no family history of the disease, has found that those with a maternal history had 15% more amyloid-beta
Both diabetes and clinical depression are known to be risk factors for dementia. Now a study that tracked nearly 4000 diabetics over 5 years has found having both increased the risk 2.7-fold.