Alzheimer’s disease tagged posts

Defective neuronal insulin sensitivity in PLB4 mice. (a) Simplified schematic showing insulin signalling. (b) Representative immunoblots of insulin-related markers in brain lysates from 8-month-old PLB4 and WT mice and (c) quantification of their relative expression. White bars, WT mice; black bars, PLB4 mice. Data are means + SEM normalised to WT values. *p < 0.05

Drugs used to treat diabetes could also be used to treat Alzheimer’s disease, and vice versa, according to new research from the University of Aberdeen. This is also the first study of its kind to show that Alzheimer’s disease can lead to diabetes, as opposed to diabetes occurring first as was previously thought...

Fibrils formed by the aggregation of the amyloid beta protein can be seen in these transmission electron microscope images, which show differences in fibril morphology between the normal protein (above) and an altered protein with one amino acid replaced by its mirror image. The altered protein also forms fibrils more slowly and is more toxic to cells. (Image credit: Warner et al., CEJ 2016)

Subtle change to amyloid beta protein affects its aggregation behavior, stabilizes an intermediate form with enhanced toxicity. Much of the research on Alzheimer’s disease has focused on the amyloid beta protein, which clumps together into sticky fibrils that form deposits in the brains of people with the disease...

One Alzheimer’s-associated mutation in the PKC protein leads to a cavity that enhances its activity. Credit: UC San Diego Health

Researchers found Protein Kinase C (PKC) alpha is necessary for amyloid beta to damage neuronal connections. They also identified genetic variations that enhance PKC alpha activity in patients with Alzheimer’s disease. The study may present a new therapeutic target for the disease. “Until recently, it was thought that PKC helped cells survive, and that too much PKC activity led to cancer. Based on that assumption, many companies tested PKC inhibitors as drugs to treat cancer, but they didn’t work,” said Prof Alexandra Newton, PhD, UC SD School of Medicine.

“Instead, we recently found that the opposite is true...

Mice with apoE4 had fewer ripples than mice with the normal apoE3 protein, and they had less slow gamma activity during the ripples. Based on these results, the scientists questioned whether these differences in activity affected the ability to form and replay memories. Image is for illustrative purposes only. Image is credited to Andrews-Zwiling Y. et al./Journal of Neuroscience, and is adapted from the Gladstone Institute video.

Scientists at the Gladstone Institutes have discovered how the major genetic risk factor for Alzheimer’s disease causes memory impairment. A specific type of brain activity important for memory replay is disrupted in mice with the E4 version of the apolipoprotein E (apoE4) gene, which may interfere with memory formation...