Lowering Tau Tips the Brain's Balance of Excitation/Inhibition
In tau knockout mice, excitatory neurons fire less; inhibitory neurons fire more. Could this dampen hyperexcitability in conditions such as Alzheimer’s?
6566 RESULTS
Sort By:
In tau knockout mice, excitatory neurons fire less; inhibitory neurons fire more. Could this dampen hyperexcitability in conditions such as Alzheimer’s?
A SARS-CoV-2 protease cleaves the transcription factor NEMO, which protects the brain's endothelial cells. In people who had COVID, and mice lacking NEMO, blood vessels shriveled. Could long COVID increase risk for dementia?
Tau PET holds a slight edge over the plasma marker in people who already have mild cognitive impairment.
The largest transcriptomic catalogue of live microglial cells to date, MiGA cinched causal connections between genetic variation, microglial gene expression, and disease.
Progranulin deficiency hyperactivates microglia, but calming these cells worsened synapse loss and neurodegeneration in mice.
Dementia risk nearly doubled after each minor stroke and tripled after each major one, regardless of vascular risk factors. Risk climbed almost sevenfold after multiple major strokes.
The data, from mice, help explain how these depressants may increase a person’s risk for dementia.
Retarding glymphatic clearance in mice caused p-tau to accumulate faster, and hastened neurodegeneration.
Peptides make lousy drugs, especially for the brain. When taken as a pill or by infusion, they either bounce off the blood-brain barrier, or get degraded within minutes...
Some people with severe COVID-19 have neurovascular injury and elevated markers of neural damage in their blood and CSF. What’s going on in their brains?
A new tracer detects α-synuclein aggregates in people with multiple system atrophy. Binding is weak, and undetectable in people with other synucleinopathies.
if Charlie Glabe is right, an exploding neuron does expel material that then triggers the formation of new, stable matter in its surroundings...
In familial AD, the faster sTREM2 rises in a person's cerebrospinal fluid, the slower his or her amyloid grows, cortex thins, and cognition fades.
Interactions with both remote and local amyloid-laden neurons drive tangles through the Alzheimer's brain. Is person-to-person variability in these interactions why patients differ in their progression?
Using a sensitive tau-PET tracer, researchers tied neuroimaging, CSF biomarkers, and cognitive symptoms to the progression of tau pathology in AD.
No filters selected