Alzheimer's disease research and treatments

This study shows that amygdala-predominant α-synuclein pathology is linked to reduced hippocampal neuron density in Alzheimer's disease, mediated through pTau and LATE-NC.

This study shows human tau modulates protein-membrane association under acute hyperglycemia, promoting glycolytic metabolism similar to the Warburg effect.

This study shows that stabilizing the retromer complex in a mouse model of Alzheimer's disease reduces Aβ production and synaptic dysfunction.

This study shows that CgA deficiency reduces tau pathology and improves cognitive function in tauopathy models by modulating epinephrine-alpha-adrenergic receptor signaling.

The paper uses CRISPR-Cas9 to edit the App gene in mice, reducing Alzheimer's disease symptoms and showing long-term benefits.

The paper identifies TYK2 as a potential therapeutic target for neurodegenerative diseases by linking cdsRNA-induced inflammation to interferon signaling and demonstrating protective effects of TYK2 inhibitors.

This study uses chemical imaging and deep learning to identify distinct amyloid plaque subtypes in Alzheimer's disease, revealing differences in Aβ composition and associations with disease progression.

This study shows that human ReNCell VM cells release tau under physiological conditions, with phosphorylation at specific sites being crucial for activity-dependent release.

This study examines 5-HT2BR expression and binding in AD mouse models and human tissue, finding age-related changes in mice and higher levels in AD patients.

The paper develops fully human bifunctional anti-tau intrabodies that reduce intracellular tau and improve neuronal survival in disease-associated mutations.

This study finds no difference in hippocampal mGluR5 levels between Alzheimer's and control brains, but shows amyloid and tau have opposing effects on mGluR5 in controls.

The paper assesses cognitive and motor function in APPSAA and APPWT mice over 12 months, finding no age-related cognitive decline but increased fecal output in APPSAA mice.

This study investigates changes in the UFMylation pathway in Alzheimer's disease brains, finding increased UFM1 conjugation and associations with pathological tau.

The paper investigates how different frequencies and durations of sensory flicker affect transcriptional profiles in 5xFAD mice, showing frequency- and duration-specific changes in immune, neuronal, and metabolic genes.

This study evaluates SNEDDS PGV-0's effects on memory and neurogenesis in mice with AD-like symptoms, finding improvements in cognitive performance and gene expression related to neurogenesis.

This study generates a conditional tau knockout model and shows that tau reduction in excitatory neurons provides excitoprotective effects, while reduction in inhibitory neurons increases seizure susceptibility, even when induced in adulthood.

The paper investigates proteome and transcriptome changes in Alzheimer's disease brains and identifies a stem cell-derived extracellular vesicle subpopulation with therapeutic potential for mitochondrial proteostasis and inflammation.

The paper maps spatial proteomic changes in dorsal and ventral hippocampus of male and female Alzheimer's disease models, identifying sex-dependent protein alterations linked to synaptic plasticity and GSK-3β activity.

This study develops a multivalent scaffold targeting LRP1 at the BBB to reduce Aβ deposits and cognitive decline in AD model mice.

This study shows that neuronal and oligodendroglial tau, but not astroglial tau, contribute to tau-PET signals in 4-repeat tauopathies.

This study identifies fibrinogen as a plasma protein binding partner for lecanemab biosimilar, suggesting it may affect drug half-life and free antibody levels in Alzheimer's disease therapy.

This study shows human APOE variants reduce both diffuse and fibrillar Aβ deposits in transgenic mouse models compared to mouse Apoe, with APOE3 more effective than APOE4 in some contexts.

The paper analyzes inter-cellular communication changes in Alzheimer's Disease using snRNA-seq and CellChat, finding conserved glutamatergic transmission changes in mice and humans.

This study shows that PLCG2 downregulation impairs synaptic function and increases Alzheimer's disease-related markers in neurons.

This study uses spatial proteomics to identify subregion-dependent protein changes in dementia variants, revealing disease-specific patterns in cortical layers and white matter.

The R136S mutation on APOE3 enhances resistance to tau-related pathology and toxicity by downregulating the cGAS-STING-IFN signaling pathway.

The paper identifies plaque-associated endogenous IgG in AD mouse models that interferes with immunohistochemical detection of mouse monoclonal IgG antibodies and shows that subclass-specific secondary antibodies can mitigate this issue.

The paper shows that adenosine deficiency in a mouse model of Alzheimer's disease leads to synaptic hyperexcitability during the asymptomatic phase, which can be restored by pharmacologic or dietary interventions.

This study shows that amyloid-beta oligomers disrupt RNA dynamics in oligodendrocytes by altering hnRNP A2 interactions, leading to increased translation of myelin proteins MBP and MOBP.

The paper identifies a Niemann-Pick type C mouse model with accelerated brain aging as a novel model for Alzheimer's disease research by analyzing transcriptomic data from congenital diseases.