Shaomin Li

Assistant professor

Brigham and Women's Hospital

United States

Research Interests

Explore related searches

Professors in United States

Contact this professor

Get a free first email built on one of their papers, ready for you to edit and send yourself.

About

Dr. Shaomin Li is an Assistant Professor at Brigham and Women's Hospital in the United States. His research focuses on the pathophysiology of Alzheimer's disease, particularly the impact of amyloid-β oligomers on synaptic function and neurodevelopment. He has contributed significantly to the understanding of metabolic disruptions and epigenetic mechanisms involved in neurodegenerative disorders, as reflected in his recent publications.

Articles (10)

Year:

2025

Year:

2025

Year:

2024

Year:

2023

Year:

2023

Year:

2023

Year:

2023

Year:

2022

Year:

2022

Year:

2020

Collaborators (2)

Gary Ho

Assistant Professor

Harvard Medical School

UNITED STATES

View details

Jens Velde Andersen

Københavns Universitet

DENMARK

View details

ApplyKite TwinLearns as you apply

Make your next move.

Prepare your application

Review drafts before you send them.

Shaomin Li

Research Interests

Explore related searches

Contact this professor

About

Articles (10)

Impairment of hippocampal long-term potentiation by soluble amyloid-β oligomers is mediated by glutamate transporter 1 expressed in neurons

Targeting epigenetic mechanisms in amyloid-β–mediated Alzheimer’s pathophysiology: unveiling therapeutic potential

Misprogramming of glucose metabolism impairs recovery of hippocampal slices from neuronal GLT‐1 knockout mice and contributes to excitotoxic injury through mitochondrial superoxide production

Increased palmitoylation improves estrogen receptor alpha–dependent hippocampal synaptic deficits in a mouse model of synucleinopathy

Soluble Aβ Oligomers Formed Channels Leading to Calcium Dysregulation

The β‐adrenergic hypothesis of synaptic and microglial impairment in Alzheimer's disease

The Relevance of Serum Macrophage Migration Inhibitory Factor Level and Executive Function in Patients with White Matter Hyperintensity in Cerebral Small Vessel Disease

Bioactive human Alzheimer brain soluble Aβ: pathophysiology and therapeutic opportunities

Disruption of the IL-33-ST2-AKT signaling axis impairs neurodevelopment by inhibiting microglial metabolic adaptation and phagocytic function

A mechanistic hypothesis for the impairment of synaptic plasticity by soluble Aβ oligomers from Alzheimer’s brain

Collaborators (2)

Gary Ho

Jens Velde Andersen

Make your next move.