JAMA Neurology reports on the differences in carriers of the “most potent genetic risk factor for Alzheimer’s disease” – the apolipoprotein E ε4 (APOE4) allele.
The updated guidelines reflect increased MCI research, the significance of MCI in clinical practice, and therapeutics in trials.
Alzheimer’s patients have brains with significantly more genetic variation than the brains of those without the disease, according to a study led by scientists at The Scripps Research Institute.
The finding may help scientists track down the mechanism that causes nearly all cases of Alzheimer’s, a mechanism that is not well understood.
A double-sided antibody targets enzyme to reduce levels of harmful amyloid-β protein in monkeys.
Additional data from the Phase III Gammaglobulin Alzheimer’s Partnership (GAP) study, including select analyses of subgroups, biomarker and imaging data, was presented at the Alzheimer’s Association International Conference (AAIC) in Boston, Massachusetts
On cognitive measures, an analysis of ApoE4 carrier patients who were treated with the 400mg/kg biweekly dose (n=87) of immunoglobulin (IG), found a statistically significant difference (p=0.012) in change from baseline in the 3MS score at 18 months versus placebo.
A team of researchers from Columbia University Medical Center (CUMC), Weill Cornell Medical College, and Brandeis University has devised a wholly new approach to the treatment of Alzheimer’s disease involving the so-called retromer protein complex.
Retromer plays a vital role in neurons, steering amyloid precursor protein (APP) away from a region of the cell where APP is cleaved, creating the potentially toxic byproduct amyloid-beta, which is thought to contribute to the development of Alzheimer’s.
A new study published in the British Medical Journal finds that anti-anxiety drugs may increase the risk of Alzheimer’s.
The drugs have been associated with short-term cognitive impairment, but the connection to Alzheimer’s has been less clear. Now, the new study finds a convincing, and apparently strong, link between benzodiazepines and Alzheimer’s disease.
A new study published in JAMA Psychiatry suggests that clinical depression is associated with a 30% increase in brain inflammation.
This finding provides the most compelling evidence to date of brain inflammation, and more specifically microglial activation, in MDE. The correlation between higher ACC TSPO VT and the severity of MDE is consistent with the concept that neuroinflammation in specific regions may contribute to sickness behaviors that overlap with the symptoms of MDE.
A new online report from the National Institutes of Health (NIH) highlights recent progress in NIH-supported Alzheimer’s disease research.
The initiatives, objectives, and advances detailed in the 2012-2013 Alzheimer’s Disease Progress Report seek to help meet the Plan’s research goal—to effectively treat or prevent Alzheimer’s disease by 2025, if not sooner.