Does Huntington’s Disease Begin in the Womb?
Tissue from 13-week-old fetuses carrying the huntingtin repeat expansion shows defects in neuronal polarity and proliferation, which lead to fewer neurons populating some brain regions.
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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.
First Primate Model of Familial AD: Marmosets with Presenilin Mutation
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.
Mitochondrial Jetsam Spurs Neurodegeneration
Spewed by stressed microglia, fragments of the organelles provoke mitochondrial fission in other cells, causing astrogliosis and neuronal loss.
Do Immune Cells in the Meninges Help with … Memory?
Resident T cells in the membrane surrounding the healthy mouse brain influence both short-term memory and synaptic plasticity.
Introducing: iPSC Collection from Tauopathy Patients
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.
Can an ApoE Mutation Halt Alzheimer’s Disease?
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.
Amyloid—It’s Not Whether, but for How Long You’ve Had It
A new study argues that the duration of a person’s amyloid positivity predicts whether they’ll develop tau accumulation and cognitive decline.
Already in Mid-30s, Poor Vascular Health Means Small Brain at 70
No link found with amyloid deposition.
Older Retired Soccer Players Prone to Neurodegeneration
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.
Lysosomal Diseases: Stepping Stones to Gene Therapy for Alzheimer’s?
While gene-based therapy for late-onset AD may seem distant, rare neurological disorders could point the way.
Chaperone Stabilizer Fends Off Amyloid, Memory Loss in Mice
A small molecule binds the retromer complex, preventing Aβ accumulation, tau hyperphosphorylation, and their downstream consequences in mice.
Toxic α-Synuclein: Egged on by ApoE4, Thwarted by ApoE2?
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.
Resilience Redefined: Sharp at Age 100, Still Sharp at 102
Centenarians who scored high on the MMSE stayed cognitively and physically active over the next two years, even if they carried genetic risk factors for Alzheimer’s. What protects these lucky few?
Traveling C9ORF72 Dipepides Jam Proteasomes in Neighboring Neurons
The slowdown of proteasomes stymied TDP-43’s entry into the nucleus and promoted its aggregation in the cytoplasm.
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