Stephen M. Strittmatter

The paper identifies a distinct receptor-bound amyloid-β filament conformation in Alzheimer's disease brain that interacts with prion protein and causes synaptic damage.

This study identifies MYO5A as a key mediator of MPS reassembly during axon regeneration, showing that ROCK-2 inhibition enhances regrowth and accelerates MPS recovery.

This study shows that a high-fat, high-sugar diet worsens cognitive deficits in Alzheimer's mouse models through metabolic stress in specific brain cells, independent of amyloid or tau pathology.

The paper investigates the neural origins of quasi-periodic patterns in resting-state fMRI using combined calcium imaging and fMRI, finding a time-locked correlation between neural activity and BOLD signals.

This paper introduces a biphasic acclimation protocol for simultaneous wide-field fluorescent Ca2+ imaging and fMRI in awake mice, showing convergent and divergent patterns in brain function between modalities.

This study identifies mGluR4 and Npdc1 as cell surface proteins that mediate α-synuclein fibril binding and neurodegeneration in Parkinson's disease models.

This study shows that ApoE2 overexpression via AAV improves axon regeneration and motor function after spinal cord injury through LRP8 signaling without affecting inflammation or scarring.

CosGeneGate selects non-redundant, cell-type-specific marker genes for single-cell analysis, outperforming existing methods in downstream applications.

This study identifies TMEM106B's role in regulating myelin lipid metabolism by interacting with galactosylceramidase in TMEM106B-deficient mice.

This study investigates the effects of repetitive mild closed-head injury on synaptic density and BOLD-fMRI signal homogeneity in mice, finding decreased synapse density and increased regional homogeneity.

The paper uses fMRI to track functional connectivity changes in a mouse model of Alzheimer's disease over time and shows that mGluR5 modulator treatment reverses these deficits.

This study shows that PrPC is necessary for synapse loss, phospho-tau accumulation, and neuronal gene expression changes in Alzheimer's knock-in mice, suggesting targeting the Aβo-PrPC interaction could prevent these pathologies.

This study shows that reduced progranulin increases tau and alpha-synuclein inclusions and worsens tauopathy mouse phenotypes via glucocerebrosidase.

This study identifies RTN4R as a regulator of ataxin-2 levels and shows its potential as a therapeutic target for ALS and SCA2.

This study identifies TMEM106B as an insoluble protein increased in MS plaques and shows its deletion causes axonal damage and lipid accumulation in demyelination models.

The paper identifies primate-specific astrocyte responses to stroke, showing NogoA limits macrophage infiltration and suggests therapeutic targeting.