Alzheimer's disease research and treatments

The paper reports cryo-EM structures of tau filaments formed in SH-SY5Y cells seeded with brain extracts from Alzheimer's and corticobasal degeneration cases, showing some structural templating.

The paper shows that ApoE4 increases Aβ42 levels in neurons and demonstrates intracellular intersection of ApoE with APP/Aβ in AD transgenic neurons.

This study examines tau expression and phosphorylation in human enteroendocrine cells, finding that tau is expressed and phosphorylated, with short chain fatty acids modulating its phosphorylation state.

The paper analyzes genomic data from early-onset and atypical dementia patients to show that both rare and common genetic variations contribute to dementia risk.

The paper uses cryo-EM to study tau filaments from Alzheimer's and CTE cases with and without flortaucipir, finding binding only in CTE Type I filaments.

This study shows that ageing-related myelin dysfunction drives amyloid-beta deposition in Alzheimer's disease mouse models, suggesting myelin integrity as an upstream risk factor.

The paper uses single-cell RNA-sequencing in Drosophila to show that tau pathology and aging affect different cell types, with tau primarily impacting excitatory neurons and glia.

The paper investigates the formation of amyloid loops in brain tissues and finds that protofibril flexibility, not hydrogen bonding, enables loop formation and disease-related toxicity.

This study uses polygenic risk scores derived from brain transcriptomic profiles to explain clinical heterogeneity in Alzheimer's disease.

The paper reports the presence of abundant Aβ fibrils in aqueous extracts from Alzheimer's disease brains, with structures identical to those in amyloid plaques.

This study examines network impairments in APPNL-G-F mice during sleep, finding NREM-specific changes in mPFC spindles and hippocampal SWRs linked to PV interneuron dysfunction.

The paper identifies sex-specific changes in cholinergic-targeting tRNA fragments in Alzheimer's disease, linking them to cholinergic neuron loss and dementia.

This study shows that tau filaments in subacute sclerosing panencephalitis and chronic traumatic encephalopathy have identical structural features.

The paper investigates GFAP-positive astrocyte responses to amyloid-beta and tau pathologies in humans and mouse models, finding distinct molecular signatures associated with each pathology.

This paper estimates SNP-based heritability of Alzheimer's disease across five cohorts, showing it ranges from 38-66%, with microglia genes explaining most of the heritability.

The paper examines brain pathologies in aging canines with and without cognitive decline, finding that tau hyperphosphorylation at T217 may predict cognitive dysfunction.

This study tests FDA-approved carbonic anhydrase inhibitors in a transgenic AD model, finding they reduce amyloid beta pathology and improve cognition by enhancing cerebrovascular health and glial function.

This study shows that TDP-43 accumulation in astrocytes impairs memory by altering antiviral pathways and chemokine signaling between astrocytes and neurons.

The paper presents a high-quality quantitative proteomics dataset for Alzheimer's disease, including samples from different brain regions and clinical groups.

The paper investigates how a haptoglobin structural variant modifies the effect of APOE alleles on Alzheimer's disease risk and age of onset in European-descent and African American populations.

This study investigates how botulinum neurotoxin A affects the release of mutant tau in hippocampal neurons, showing it blocks mutant tau release by modulating SNAP25.

This study shows that visual evoked potentials change in early tauopathy, suggesting they could be a biomarker for early disease stages.

This study shows that human neurons lacking APP have developmental and presynaptic deficits that are corrected by cholesterol, suggesting APP's role in maintaining cholesterol homeostasis for brain function.

The paper determines that tau and TMEM106B filaments from gray and white matter in MSTD have identical folds.

The paper introduces EMBER, a spectral imaging method using machine learning to identify amyloid strains in neurodegenerative diseases.

This study shows BMAA affects neuroblastoma and glioblastoma cells through distinct mechanisms, including Wnt pathway modulation and a Wnt-independent pathway, suggesting potential therapeutic targets.

The paper investigates how synthetic torpor induces reversible Tau hyperphosphorylation in rats, revealing a regulated neuroprotective mechanism involving metabolic and inflammatory changes.

This study identifies shared genetic pathways between Alzheimer's disease, aging, and longevity using gene set enrichment analysis and validates them with statistical significance.

The paper shows that CCR5 deficiency reduces TIMP levels, improves gamma oscillation power, and enhances learning in APOE4 mice.