A drug candidate for Alzheimer’s aims to make cell trafficking more efficient, reduce Aβ production.
A new study charges that, contrary to previous studies, seeding the mouse brain with aggregated α-synuclein does not trigger a toxic spread of PD-like inclusions in wild-type mice.
Scientists had the good fortune to study the exceedingly rare instance of a pair of identical twins, only one of whom had Trisomy 21. It turned out that gene regulation was altered across the entire genome in the twin with Down’s syndrome.
Allegations of scientist misconduct led to the retraction of one high-profile stem cell paper and put two others in doubt.
A small molecule inhibitor kills all microglia in the brain, but the cells rapidly repopulate from a previously unidentified progenitor cell.
If new results hold up, enhanced phosphorylation of a ribosomal protein may explain the toxicity of mutations that cause Parkinson's.
A new bill will centralize the approval process for multinational trials and mandate the publication of trial results—good or bad.
A new bill asks Congress to ramp up Alzheimer’s funding by breaking down the cost to meet each of the milestones in the national plan. It appropriates no funds.
Older adults with amyloid in their brains develop abnormal activity in the entorhinal cortex even while memory and hippocampal function remain unaffected.
The April issue of Health Affairs is dedicated to Alzheimer’s. Authors gathered in Washington, D.C., to articulate how world policy could take shape.
As the adage goes, an ounce of prevention is worth a pound of cure. A new journal aims to find out if this is true for Alzheimer’s.
A new link between two proteins tied to Parkinson’s has implications for the disease and beyond.
Scientists have come around to the idea that the consequences of Down's syndrome extend beyond the additional copy of chromosome 21. However, because natural genetic variation among people obscures subtle changes in gene expression, they have been unable to pinpoint exactly how other chromosomes are affected. Now, by studying an extremely rare set of identical twins—one with trisomy 21 and the other without—researchers report that natural swings in gene expression are tempered in Down's. Genes that are usually highly expressed quiet down, while those that are normally silent became more active. The study suggests that Down’s causes genome-wide epigenetic changes.
Do microglia help or harm a diseased brain? Researchers have a new tool to investigate. In the April 16 Neuron, scientists report that they can remove all microglia from wild-type mice with a small molecule. The animals remain healthy, and as soon as the inhibitor is withdrawn, new microglia sprout from a previously unidentified progenitor cell, repopulating the brain within days. The method will allow studies of what these immune cells do in disease and injury. It could also have therapeutic potential as a means to dampen inflammation or replace sick microglia with healthy ones.
Mice run rampant through the Alzheimer’s disease literature, providing valuable insight despite their many limitations as models of human disease. Why do some models develop certain pathologies while others do not? Which models are best suited for a particular line of investigation? To help you answer these and other questions, Alzforum has curated data on nearly 100 mouse models, with more to come. For each entry, we highlight key features in interactive graphics and customizable tables that make models easy to compare and contrast. In addition, we plot age at onset of core phenotypes, such as plaques, tangles, and cognitive impairment, in interactive diagrams of the murine lifespan. Check out this new resource and tell us what you think.
In Alzheimer's disease, preclinical hopes too often have been dashed by clinical failure. While amyloid plaques can be cleared and memory restored in mice, the same is not yet true for people. Are mice too different, or do the models lack a certain je ne sais quoi? Researchers led by Takaomi Saido at RIKEN, Japan, have created a different type of model. These APP knock-ins make human Aβ from the mouse APP locus and develop amyloid pathology without overexpressing APP or any of its other cleavage fragments. Those pile up in mice expressing human transgenes, muddling interpretation of the various phenotypes. In this initial paper, Saido started comparing the knock-ins to two overexpression lines. He offers to share his mice broadly with other labs. Compare Saido’s and older APP strains on Alzforum’s new Research Models database, then join Saido at noon U.S. Eastern time on Tuesday, April 22, for a discussion with leaders in the field.
Some scientists are developing Alzheimer’s drugs that remove Aβ or block enzymes that produce it. Others are taking a different tack—stabilizing cellular processes that protect against the disease. With help from computer simulations, researchers found a small molecule that bolsters the retromer, a protein machine that steers the amyloid precursor protein away from the enzyme that initiates production of Aβ. Dubbed R55, the compound reduced Aβ in mouse neurons.
- Olav Andersen on Could Bolstering the Retromer Thwart Alzheimer’s?
- Matthew M J Farrer on Could Bolstering the Retromer Thwart Alzheimer’s?
- Samuel Gandy on Could Bolstering the Retromer Thwart Alzheimer’s?
- James J. Lah on Could Bolstering the Retromer Thwart Alzheimer’s?
- Marc Diamond on Amyloidogenic α-synuclein seeds do not invariably induce rapid, widespread pathology in mice.
- Saak Ovsepian on Neuronal activity regulates extracellular tau in vivo.
- Michael Lardelli on Novel presenilin mutations within Moroccan patients with Early-Onset Alzheimer's Disease.