Can an Antibody Allele Boost Your Alzheimer’s Risk By Giving Herpes an Edge?
Homozygous carriers of GM17—a common IgG1 variant the HSV-1 virus has evolved to evade—had quadruple the risk of developing AD. In a small Swedish cohort, that is.
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Homozygous carriers of GM17—a common IgG1 variant the HSV-1 virus has evolved to evade—had quadruple the risk of developing AD. In a small Swedish cohort, that is.
Three young monkeys missing exon 9 of presenilin 1 seem to have an elevated Aβ42/40 ratio. It remains to be seen if they will develop plaques and tangles as they age.
Sedentary mice infused with the plasma of active ones had more newborn neurons in the brain and less neuroinflammation. Exercising upped plasma clusterin in mice and in humans.
Spewed by stressed microglia, fragments of the organelles provoke mitochondrial fission in other cells, causing astrogliosis and neuronal loss.
A new study argues that the duration of a person’s amyloid positivity predicts whether they’ll develop tau accumulation and cognitive decline.
The circular transcripts correlate with AD pathology and dementia severity, suggesting potential roles in pathogenesis or as biomarkers.
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.
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.
No link found with amyloid deposition.
While gene-based therapy for late-onset AD may seem distant, rare neurological disorders could point the way.
A small molecule binds the retromer complex, preventing Aβ accumulation, tau hyperphosphorylation, and their downstream consequences in mice.
Quite independently of what it does to Aβ or tau, ApoE4 stokes α-synuclein pathology in mouse models. People with Lewy body dementia who carry ApoE4 had more phosphorylated synuclein in their brains, and their cognition declined faster.
Post-translational modifications differ from those in AD tau fibrils, and may dictate tau strains.