Hypometabolism in the frontal cortex and in the anterior default mode network distinguish the behavioral variant of AD from typical AD.
Overexpressing neuronal A2A receptors stoked C1q in microglia, damaging synapses and memory.
Ablating the immune cells protected mouse models of frontotemporal dementia from the neurodegeneration caused by human ApoE4.
Imaging studies suggest that ApoE4 carriers may be more susceptible to the effects of tangles, particularly if they are women.
The first ever cryoEM structures of Aβ fibrils extracted from AD tissue look quite different than prior structures of fibrils generated in vitro. For starters, they are right-hand twisted, not left-hand.
Spewed by stressed microglia, fragments of the organelles provoke mitochondrial fission in other cells, causing astrogliosis and neuronal loss.
Resident T cells in the membrane surrounding the healthy mouse brain influence both short-term memory and synaptic plasticity.
The resource boasts 56 stem cell lines derived from tau mutation carriers, patients with sporadic disease, healthy controls, and engineered isogenic lines, including some that have their mutation corrected by CRISPR.
The rare ApoE3 Christchurch variant prevented tau tangles, neurodegeneration, and cognitive decline in a woman’s brain for decades, despite massive amyloid buildup from a familial presenilin AD mutation.
A new study argues that the duration of a person’s amyloid positivity predicts whether they’ll develop tau accumulation and cognitive decline.
No link found with amyloid deposition.
While former professional soccer players have less risk for heart disease and cancer than the general population, they are five times more likely to die with a neurodegenerative disease in old age.
While gene-based therapy for late-onset AD may seem distant, rare neurological disorders could point the way.
The circular transcripts correlate with AD pathology and dementia severity, suggesting potential roles in pathogenesis or as biomarkers.
The pattern varied from person to person, depending on the site of injury, in contrast to the stereotyped distribution of tau tangles seen in Alzheimer’s disease.