Alzheimer's disease research and treatments

The paper evaluates the association of Apolipoprotein E4 allele with neurodegenerative diseases in Eastern Indians, finding significant links with disease subtypes, age at onset, and family history.

The paper performs a genome-wide meta-analysis of CSF biomarkers in Alzheimer's and Parkinson's disease cohorts to identify genetic associations and disease-specific patterns.

The paper identifies small molecules that inhibit proteotoxicity and inflammation in Alzheimer's Disease models, revealing mechanisms linking glycolysis to neuroinflammation and suggesting new therapeutic targets.

The paper identifies early and selective subcortical Tau pathology in the Papez circuit, particularly in the anterodorsal thalamic nucleus, and links it to disorientation in dementia.

The paper identifies a transient hyperactive neuronal state in early Alzheimer's disease using single-nucleus transcriptomics from living patients.

This study develops isogenic iPSC lines with MAPT S305 mutations to increase 4R tau expression, revealing altered neuronal and astrocytic functions in tauopathies.

This study shows that expressing human amyloid-β and Tau in C. elegans neurons causes phenotypic and multi-omic changes, including accelerated aging and metabolic dysfunction.

The paper uses in vivo protein footprinting to study dynamic conformational changes in the proteome across multiple tissues in Alzheimer's disease progression, finding that structural changes precede expression changes in key pathways.

The paper uses whole-brain imaging to show that tau pathology in mice propagates retrogradely through brain networks.

This paper develops a deep learning pipeline to automate amyloid pathology quantification in Alzheimer's disease, achieving human-level accuracy and enabling high-throughput analysis.

This study shows that SARS-CoV-2 infection causes Tau phosphorylation and aggregation in neurons, linked to Alzheimer's disease pathology.

This study uses molecular simulations to compare substrate preferences between PS1 and PS2 γ-secretase enzymes for APP and Notch1 processing, revealing differences in conformational flexibility and binding energy.

The paper uses scRNA-seq data to identify gene expression rewiring in Alzheimer's Disease linked to risk variants by analyzing differential correlations across cell types.

This study uses single-nucleus multi-omics data to identify cis and trans regulatory networks and their target genes in Alzheimer's disease brains.

The paper shows transcript errors generate amyloid and prion-like proteins in human cells, linking DNA damage to aging and disease.

This study characterizes the effects of Aβ1-42 injection on memory and synaptic plasticity in male and female mice, finding long-lasting impairments in both sexes.

The paper examines mossy fiber BDNF protein stability in AD mouse models and finds it remains unchanged with age, correlating with neuronal activity and resistance to amyloid-beta accumulation.

This study shows that Neat1 overexpression in astrocytes of male AD mice contributes to memory deficits by promoting astrocyte dysfunction, not through neuronal activity changes.

This study uses cryo-EM to show that tau filaments in ALS/PDC share the CTE fold, suggesting environmental causes for the disease.

This study compares synaptic proteomes from a Down syndrome mouse model and Alzheimer's disease patients, identifying shared alterations that may underlie common pathological mechanisms.

This study tests a combination of secondary plant metabolites and micronutrients in an Alzheimer's disease cell model, finding some beneficial effects but not all desired outcomes.

The paper tests the effects of coffee constituents on mitochondrial dysfunction and amyloid beta in an Alzheimer's cell model, finding increased ATP and pyruvate levels with some substances.

The paper compiles and analyzes proteomic data from 38 Alzheimer's disease studies to create a database of protein changes in human brain tissue across disease stages and regions, revealing patterns of protein dysfunction.

This paper evaluates 53 Tau antibodies for Western blot and immunohistochemistry, identifying those with high specificity and sensitivity for detecting Tau, including low-level and modified forms.

This study identifies an Alzheimer's disease-specific cytokine signature that suppresses mitochondrial function in neurons, linking neuroinflammation to metabolic dysfunction.

This study shows that m6A accumulation correlates more strongly with MAPT pathology than beta-amyloid in an Alzheimer's mouse model.

This study shows that AD astrocytes have reduced mitochondrial and glycolytic function, which can be improved by increasing hexokinase 1 expression.