People with Alzheimer’s disease who were treated with diabetes drugs showed considerably fewer markers of the disease including abnormal microvasculature and disregulated gene expressions in their brains compared to Alzheimer’s patients without treatment for diabetes, Mount Sinai researchers report. Results of the study will be published in PLOS One online on November 1st at 2PM. This is the first study to examine what happens in the pathways of both brain tissue and endothelial
(Reuters) - Eisai Co Ltd and Biogen Inc will move forward with late-stage clinical trials of their Alzheimer’s disease drug, BAN2401, and are working with regulators to design the next studies and gain expedited review as a breakthrough therapy. The companies announced this month that despite failing at an earlier stage, the drug slowed Alzheimer’s progression at its highest dose, providing renewed hope in a field littered with failures. In
(REUTERS) Japanese drugmaker Eisai Co and Biogen Inc said that the final analysis of a mid-stage trial of their Alzheimer’s drug showed positive results for patients who received the highest dose. The news sent Eisai’s shares up as much as 14.6 percent in Friday morning trading in Tokyo while Biogen’s shares were up 7 percent at $320 in after-hours trading. The companies said in a July 5 statement the highest
Years before people start showing characteristic symptoms of Alzheimer’s disease, sticky plaques begin forming in their brains, damaging nearby cells. For decades, doctors have sought ways to clear out these plaques as a way to prevent or treat the disease. The sticky clumps, known as amyloid plaques, are composed primarily of a brain protein called amyloid beta. But nestled within the plaques are small amounts of another Alzheimer’s protein: APOE.
Writing in the April 11 issue of The Journal of Clinical Investigation, researchers at University of California, San Diego School of Medicine say abnormalities in a protein that helps transport and sort materials inside cells are linked to axonal dysfunction and degeneration of neurons in Alzheimer’s disease (AD) and Down syndrome (DS). “Amyloid plaques and neurofibrillary tangles in the brain are hallmarks of AD patients and people with DS. However,