Alzheimer's disease research and treatments

The paper develops a mechanistic model of tau protein dynamics using PET data to predict regional tau accumulation and disease progression stages in Alzheimer's patients.

This study characterizes stress granule structural and molecular changes in Alzheimer's disease subtypes using multi-omics approaches, revealing distinct features in rapidly progressive AD.

This study uses nanospectroscopy to analyze how anti-amyloid antibodies affect Aβ-42 protein aggregates, finding differences in oligomer reduction and fibril formation between aducanumab and lecanemab.

The paper shows APP and Aβ-peptides modulate protein aggregation and DCG biogenesis in Drosophila cells, with mutant Aβ-peptides disrupting these processes and causing AD-like pathologies.

This study determines the cryo-EM structures of Aβ40 and medin fibrils in vitro, revealing polymorphic remodeling and mixed amyloid interactions.

The paper uses spatial transcriptomics to analyze Aβ plaques and glial interactions in AD brains, finding that low Aβ areas show more neuronal loss and high-glia areas show inflammation and neurodegeneration.

This paper uses an interpretable deep learning framework to analyze transcriptomic data from Alzheimer's disease brain tissues, identifying gene signatures and sex-specific modules associated with microglia activation and neuronal loss.

This study investigates the genetic overlap between inflammatory bowel disease and Alzheimer's disease, finding distinct myeloid cell-specific risk factors and some protective associations.

This paper develops a genetically encoded biosensor to detect and select amyloid-β oligomer binders, identifying new binders more effective than existing ones at delaying secondary nucleation.

This study investigates the structural characteristics of amyloid-beta aggregates in cerebral amyloid angiopathy, identifying antiparallel beta-sheet structures linked to lipid-mediated aggregation.

This study shows that amyloid-beta fibrils catalyze ATP hydrolysis, leading to calcium phosphate crystallization, which may explain calcification in Alzheimer's disease.

This study shows that anionic lipids like DMPG influence insulin aggregation pathways and intermediate formation, with soluble intermediates being more cytotoxic than fibrils.

This study shows that iron promotes Aβ fibrillization and synergizes with Aβ to cause neuronal death in an ex vivo AD model.

The paper identifies cell-type-specific metabolic regulators in Alzheimer's disease using scFUMES, revealing key interactions that reduce pathological tau species.

This study develops an analytical model to describe lipid-induced protein aggregation kinetics, capturing both one-step and two-step nucleation mechanisms and predicting key kinetic observables.

The paper examines apoE glycosylation in CSF and plasma samples from ADNI, finding reduced glycosylation in MCI and progressors, and associations with AD biomarkers like t-tau, p-tau181, and Aβ1-42.

This study shows that amyloid accumulation in medial septal cholinergic neurons of aging mice leads to REM sleep loss, cognitive and emotional deficits, and amyloid spread to other brain regions.

This study uses AAV-based gene therapy to replace APOE4 with APOE2 in mice, revealing that long-term replacement reverses AD pathology while short-term replacement worsens it, with RAB24 playing a key role.

This study shows that TDP-43 and Tau directly interact, promoting co-condensation but reducing Tau fibril formation and seeding.

The paper investigates how metabolites linked to type 2 diabetes and Alzheimer's disease affect intracellular signaling in mouse neurons, identifying specific pathway activations associated with disease progression or protection.

The paper uses snRNA-seq in Drosophila to study how AD-associated proteins affect peripheral tissues, finding distinct impacts of Aβ42 and Tau on sensory neurons and non-neuronal tissues.

This study identifies miR-501-3p and miR-502-3p as potential biomarkers for Alzheimer's disease by showing their upregulation in AD-related samples.

The paper identifies impaired hippocampal circuit function in a mouse model of Alzheimer's disease before Aβ deposition, highlighting issues in theta-gamma oscillations and place cell reactivation during sleep.

This study identifies initial cleavage sites of γ-secretase substrates NRG1 and CDH1 and confirms the phenylalanine rule at the P2 position.

This study shows that exercise or donepezil treatment can reduce proteomic changes in sciatic nerves of 5xFAD mice, preserving neuromuscular function before cognitive decline.

The paper identifies Gbp2b as an early biomarker of tauopathy in the olfactory epithelium of PS19 mice through transcriptomic analysis across different ages.

This study identifies neuronal lysosomal acid lipase (LAL) loss as a driver of amyloid pathology in Alzheimer's disease by linking disrupted lipophagy to Aβ accumulation and cognitive deficits.

This study examines the interactions between A{beta}, tau, LATE-NC, -synuclein, and APOE {varepsilon}4 in 480 post-mortem brains, finding that tau is the strongest predictor of neurodegeneration while LATE-NC primarily affects hippocampal neuron loss.

This study shows that long-term antiplatelet therapy with clopidogrel reduces cerebral amyloid angiopathy and soluble Aβ42 levels but not parenchymal amyloid plaques or neurodegeneration in APP23 mice.

This paper presents a single-domain antibody-based protein degrader that reduces tau levels and improves motor function in tauopathy models.