Alzheimer's disease research and treatments

The paper identifies epigenetic and gene expression changes in mice exposed to prolonged low-dose Aβ42, linking them to phases of memory enhancement, transition, and decline associated with Alzheimer's disease.

This study shows that BIN1 isoform 1 expression in the presynaptic compartment causes synaptotoxicity, leading to synaptic loss and structural changes in Drosophila and rat models.

This study shows that tau accumulation leads to neuronal silencing and network dysfunction in the hippocampal formation without neuron loss, contributing to progressive network disruption.

This study shows HSV-1 infection increases cofilin phosphorylation in 5xFAD mice, linking viral infection to AD pathology through actin cytoskeleton disruption.

This study shows that tau phosphorylation patterns influence microtubule stability, with specific phosphorylations impairing tau's ability to counteract destabilization, suggesting phosphorylation may respond to, rather than precede, MT instability.

This study shows that manual lymph drainage massage of the head and neck improves cognition and reduces Aβ and NfL levels in 5x-FAD mice.

This study shows that tau deletion enhances synaptic weakening in male rats but not females, revealing sex-dependent effects on synaptic function and actin dynamics.

The paper detects an unfolded p53 conformation (U-p53AZ) in Alzheimer's disease brain samples, showing colocalization with pTau in neurofibrillary tangles.

This paper investigates how Ac-BIM-acid affects amyloid fibril morphology of Stm1_N1-113 and Aβ42 using AFM and NMR, showing structural modulation at different concentrations.

This study shows human tau disrupts neuronal structure in C. elegans, with effects worsened by age, stress, and phosphorylation.

The paper investigates the role of tau in VTA dopamine neuron dysfunction in Alzheimer's disease models, finding that tau induces hyperexcitability but impairs burst firing.

This study investigates the effects of the SORL1 p.Y1816C variant on neuronal function using iPSC-derived models, showing impaired SORLA maturation, altered APP processing, and disrupted axonal transport and electrophysiology.

This study identifies CD45 as a sialic acid-dependent binding partner of CD33, showing that their interaction contributes to Alzheimer's disease susceptibility through impaired microglial function.

This study investigates how tau pathology affects metabolism and excitatory activity in mouse models, finding that it preserves glucose tolerance and shifts metabolic flux toward glutamate synthesis.

This study shows that endomorphins and sitagliptin improve amyloid-beta clearance and memory in an Alzheimer's cell model by reducing oxidative stress and Aβ42 aggregation.

This study shows Lecanemab reduces amyloid pathology by activating microglia through Fc fragment engagement, enhancing phagocytosis and lysosomal degradation.

This study identifies nervous system requirements for Alzheimer's disease risk genes in Drosophila by analyzing gene function and neurodegeneration.

The paper shows that platelets from early-stage Alzheimer's patients bind more amyloid-beta, have altered morphology, and show sex-specific activation differences, suggesting potential as biomarkers for AD.

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.

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

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 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.

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.

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.