Dr. Laibaik Park

A new study by Weill Cornell Medicine researchers helps explain why having ApoE4—the gene variant most closely linked to Alzheimer’s disease—increases the risk of neurodegeneration and white matter damage. 

Researchers at Weill Cornell Medicine have demonstrated how amyloid beta, a peptide associated with Alzheimer’s disease, can interact with a protein receptor on immune cells in the brain triggering a reaction that damages blood vessels and leads to neurodegeneration. 

Abnormal forms of a brain-cell protein called tau, which have long been implicated in Alzheimer’s and other neurodegenerative disorders, may contribute to neurodegeneration earlier than was previously understood, by interfering with the normal dynamics of blood flow in the brain.

A protein linked to both Alzheimer’s disease and a form of dementia increases the risk of cognitive impairment by reducing the number and responsiveness of blood vessels in the organ.

By studying the effects of immune cells that surround blood vessels in the brain, Weill Cornell Medicine researchers have discovered a new pathway involving these cells that may contribute to the cause of Alzheimer’s disease.