Astrocytes Agitate Neurons in Huntington’s Disease
Astrocytes kindle neuronal hyperexcitability in mouse models of Huntington’s.
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Astrocytes kindle neuronal hyperexcitability in mouse models of Huntington’s.
When a calcium sensor disappears from dendritic spines, synapse loss soon follows in Alzheimer’s models, aging mice, and diseased human brains.
The most detailed connectivity map for the mammalian brain to date will allow investigators to track neuronal networks at an unprecedented scale.
A new link between two proteins tied to Parkinson’s has implications for the disease and beyond.
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.
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.
Older adults with amyloid in their brains develop abnormal activity in the entorhinal cortex even while memory and hippocampal function remain unaffected.
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.
A new bill will centralize the approval process for multinational trials and mandate the publication of trial results—good or bad.
If new results hold up, enhanced phosphorylation of a ribosomal protein may explain the toxicity of mutations that cause Parkinson's.
A small molecule inhibitor kills all microglia in the brain, but the cells rapidly repopulate from a previously unidentified progenitor cell.
Allegations of scientist misconduct led to the retraction of one high-profile stem cell paper and put two others in doubt.
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.
Nucleotide repeat expansions in the C9ORF72 gene occur in amyotrophic lateral sclerosis and frontotemporal dementia. Now researchers find the same repeats in patients with two other neurological disorders.
New research suggests that dendritic tau may participate in synaptic plasticity, and that Aβ disrupts this function.