On The Docket at AD/PD: The Many Crimes of ApoE4
Microglia cleanup, mitophagy, axonal plasticity, blood-brain barrier. A renewed focus on ApoE4 is revealing new ways in which this isoform renders the brain vulnerable to Alzheimer’s.
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Microglia cleanup, mitophagy, axonal plasticity, blood-brain barrier. A renewed focus on ApoE4 is revealing new ways in which this isoform renders the brain vulnerable to Alzheimer’s.
In a research study, one-fifth of healthy people who learned they were at high risk for AD said they might consider physician-assisted death as a future option.
“We are learning” was the tenor of debate about the latest round of setbacks for anti-amyloid trials in symptomatic Alzheimer’s disease at a recent conference in Lisbon.
Chemotherapy riles microglia, causing neurons to turn down expression of BDNF, a growth factor necessary for myelination. Restoring BDNF signaling on oligodendrocytes spared myelin and memory loss.
Much of the neuron loss in rTg4510 mice comes from accidental disruptions in mouse genes rather than expression of mutant tau. Pathology spreads quickly in human tau knock-ins.
Analyzing Phase 2 trial CSF of an investigational immunotherapy, scientists showed for the first time that treatment mitigates neurotoxic oligomers in patients.
In early Parkinson’s disease, sparse areas on the retina correlate with dying dopaminergic neurons in the substantia nigra.
A batch of new monoclonal antibodies against the C9ORF72 protein also revealed the protein lingers in presynapses.
Tau-laden neurons present a phospholipid “eat me” signal, bidding microglia to devour them alive.
Neural-wave patterns could help clinicians guide electrodes for deep-brain stimulation.
With buckets of new data at AAIC, blood NfL grabbed attention as a telltale of neurodegeneration. The protein predicts progression, and might one day track treatment effects.
AAIC showcased advances in scientists’ attempts to integrate technology into dementia care and research. This includes the use of furry robot seals to keep patients company.
Loss-of-function mutations in TBK1 combined with age-related dearth of an analog spell trouble for motor neurons and the central nervous system.
PET tracer predicts tau pathology and AD, according to company press release.
A new finding questions the usefulness of some mouse models.