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.
The most detailed connectivity map for the mammalian brain to date will allow investigators to track neuronal networks at an unprecedented scale.
Hardening of the arteries correlated with greater amyloid deposition in a longitudinal study, strengthening ties between cardiovascular disease and Alzheimer’s.
When a calcium sensor disappears from dendritic spines, synapse loss soon follows in Alzheimer’s models, aging mice, and diseased human brains.
IMAGINE that: Amyloid deposition shrinks in both treatment and placebo groups, dealing a blow to the anti-aggregation drug PBT2.