Michael K. Lee

Internalized α-synuclein fibrils become truncated and resist degradation in neurons while glial cells rapidly degrade α-synuclein fibrils.

This study shows neurons inefficiently metabolize internalized α-synuclein fibrils, which become truncated and resist degradation, while glial cells rapidly degrade them.

UNC-45A Drives ATP-Independent Microtubule Destabilization via Defect Recognition and Repair Inhibition Contributing to Neurite Dystrophy

This study identifies UNC-45A as an ATP-independent microtubule severing protein that inhibits repair of defects, leading to microtubule loss and neurite dystrophy in Alzheimer's disease.

Protein kinase CK2 alpha prime as a dual modulator of neuroimmune signaling and synaptic dysfunction in Tauopathy

This study identifies CK2 as a regulator of tauopathy by modulating tau phosphorylation, neuroinflammation, and synaptic dysfunction in mice.

Oral prodrug of a novel glutathione surrogate reverses metabolic dysregulation and attenuates neurodegenerative process in APP/PS1 mice

This paper evaluates a prodrug of a glutathione surrogate in an Alzheimer's mouse model, showing it reduces oxidative stress, amyloid pathology, and neurodegeneration while identifying metabolic biomarkers.

UNC-45A is Highly Expressed in the Proliferative Cells of the Mouse Genital Tract and in the Microtubule-Rich Areas of the Mouse Nervous System

The paper identifies UNC-45A expression in proliferative cells of the mouse genital tract and microtubule-rich areas of the nervous system, suggesting its potential role in ovarian cancer and neurodegeneration.

Partial inhibition of mitochondrial complex I attenuates neurodegeneration and restores energy homeostasis and synaptic function in a symptomatic Alzheimers mouse model

The paper shows that partial inhibition of mitochondrial complex I protects against neurodegeneration in Alzheimer's mice by improving energy homeostasis, synaptic function, and reducing inflammation.