Andrew A. Sproul

Reduced SH3RF3 may protect against Alzheimer's disease by lowering microglial pro-inflammatory responses via modulation of JNK and NFkB signaling

The paper identifies protective SH3RF3 variants that delay Alzheimer's onset by reducing microglial inflammation through JNK and NFkB pathway modulation in PSEN1G206A carriers.

High throughput identification of genetic regulators of microglial inflammatory processes in Alzheimer's disease

This study identifies genetic regulators of microglial inflammation in Alzheimer's disease using CRISPRi screens and scRNA-seq, revealing key genes that modulate inflammatory states and disease-relevant clusters.

A proteogenomic tool uncovers protein markers for human microglial states

The paper introduces a proteomic tool to identify protein markers for human microglial states and validates their utility in purification and differentiation.

HDAC Inhibitors recapitulate Human Disease-Associated Microglia Signatures in vitro

The paper uses HDAC inhibitors to mimic human DAM in vitro and identifies shared marker genes.

Generation of hiPSC-derived brain microvascular endothelial cells using a combination of directed differentiation and transcriptional reprogramming strategies

This paper generates and characterizes reprogrammed brain microvascular endothelial cells from hiPSCs using transcription factors FOXF2 and ZIC3, showing improved BBB properties and integration with neural cells in a 3D system.

A pharmacological toolkit for human microglia identifies Topoisomerase I inhibitors as immunomodulators for Alzheimer's disease

The paper identifies Topoisomerase I inhibitors as immunomodulators for Alzheimer's disease by characterizing their effects on human microglial subtypes in vitro and in a zebrafish model.

ZCCHC17 modulates neuronal RNA splicing and supports cognitive resilience in Alzheimer's disease

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

Aβ42 oligomers trigger synaptic loss through CAMKK2-AMPK-dependent effectors coordinating mitochondrial fission and mitophagy

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

NSun2 deficiency promotes tau hyperphosphorylation and neurodegeneration through epitranscriptomic regulation of miR-125b

This study shows NSun2 deficiency in AD leads to miR-125b dysregulation and tau hyperphosphorylation, promoting neurodegeneration through epitranscriptomic mechanisms.

Impaired α-tubulin re-tyrosination leads to synaptic dysfunction and is a feature of Alzheimer's disease

THE C99 FRAGMENT OF APP REGULATES CHOLESTEROL TRAFFICKING

This study shows that the C99 fragment of APP regulates cholesterol trafficking between the plasma membrane and ER, contributing to AD pathogenesis.

A CRISPR/Cas9 based strategy to manipulate the Alzheimer’s amyloid pathway

This paper introduces a CRISPR/Cas9 strategy to edit APP and manipulate the amyloid pathway in Alzheimer's disease by reducing β-cleavage and Aβ while increasing α-cleavage.