Annie Lee

This paper identifies APOE-ϵ4-induced fibronectin accumulation at the blood-brain barrier as a key mediator of astrocyte-endothelial dysfunction in Alzheimer's disease, highlighting it as a potential therapeutic target.

This study shows how non-coding variants in CD33 affect Alzheimer's risk by altering CD33M dimerization and interactions with clusterin and Aβ, impacting microglial function.

This study identifies molecular programs distinguishing vascular, neurodegenerative, and mixed pathology in aging human brains using proteomic and transcriptomic data.

The paper identifies sex- and Alzheimer's disease stage-specific genetic regulators of plasma metabolites and their associations with biomarkers.

This paper develops an APOE-independent polygenic risk score for Alzheimer's disease that shows associations with cognitive decline and neuropathological markers across diverse populations.

TPClust integrates longitudinal phenotypes with high-dimensional omics data to identify subtypes with distinct cognitive trajectories and risk profiles in aging populations.

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.

The paper shows biological age and age acceleration in blood predict Alzheimer's disease plasma biomarker levels in a Hispanic cohort.

The paper uses single-cell data to identify factors regulating an Alzheimer's disease-related microglial signature and proposes a new analytic framework for microglial classification.

This study shows that mitochondrial DNA removal is essential for sperm development and activity, revealing a novel exonuclease, ExoA, required for mtDNA elimination and preventing nuclear-mito imbalance.

The paper identifies a transcriptional network regulating mitochondrial biogenesis in Drosophila by combining RNAi screening and ChIP-seq analysis, revealing key factors like CG1603 and YL-1.

The paper examines immunosenescence trajectories in diverse populations, finding associations between immunological age and brain atrophy, while highlighting CMV status and genetic ancestry as key factors.

This study links psychosocial experiences to mitochondrial biology in the human brain, finding positive experiences correlate with higher OxPhos machinery abundance and negative experiences with lower abundance.

The paper analyzes bulk RNA-seq data from diverse ethnic groups to identify differentially expressed genes and pathways in Alzheimer's Disease, highlighting cross-ethnic and ethnic-specific findings.

This study develops an image segmentation pipeline to analyze human microglia morphology in Alzheimer's disease, revealing that microglia associated with amyloid plaques have distinct morphological features.

This study shows ZCCHC17 regulates RNA splicing in neurons and its dysfunction contributes to splicing abnormalities in Alzheimer's disease, with potential therapeutic implications.

The paper shows that Ngfr promotes neurogenesis and reduces amyloid pathology in AD mouse models by suppressing Lcn2/Slc22a17 signaling.

This study identifies and validates two molecular subtypes within early and late mild cognitive impairment stages of Alzheimer's disease using integrated metabolomics and transcriptomics data.

The paper identifies two subtypes of aging brains with distinct Alzheimer's risk profiles and differential impacts of APOEε4.

This study shows Aβ42 oligomers cause synaptic loss by activating CAMKK2-AMPK, which coordinates mitochondrial fission and mitophagy in neurons.

This study identifies disease-enriched microglial subsets and validates compounds that modulate their states using single-cell RNA sequencing and in vitro experiments.