July 6, 2024
Amyloid Plaques

Manipulating Cellular Interactions Around Amyloid Plaques: A Novel Approach to Slowing Down Alzheimer’s Disease Progression

Researchers at the Icahn School of Medicine at Mount Sinai have recently published a groundbreaking study in Nature Neuroscience, shedding light on potential new strategies to combat Alzheimer’s disease. The team, led by Roland Friedel, Ph.D., and Hongyan Zou, Ph.D., discovered that targeting the plexin-B1 protein and reactive astrocytes could enhance the brain’s capacity to eliminate amyloid plaques, a key feature of Alzheimer’s.

The study focuses on the critical role of reactive astrocytes, a type of brain cell that becomes activated in response to injury or disease, in controlling the spacing around amyloid plaques. These cells influence how other brain cells can access and clear these harmful deposits.

Friedel, an Associate Professor of Neuroscience and Neurosurgery at Icahn Mount Sinai, stated, “Our findings suggest a promising avenue for developing new treatments by optimizing how cells engage with these detrimental plaques.” The research was inspired by the examination of intricate data comparing healthy individuals to those with Alzheimer’s, with the goal of uncovering the molecular and cellular underpinnings of the disease.

Zou, a Professor of Neurosurgery and Neuroscience at Icahn Mount Sinai and one of the study’s lead authors, emphasized the broader implications of their findings. “Our study paves the way for Alzheimer’s research, underscoring the significance of cellular interactions in creating effective neurodegenerative disease therapies,” she said.

By manipulating the plexin-B1 protein, researchers may be able to improve the brain’s ability to eliminate amyloid plaques, potentially slowing down or even halting the progression of Alzheimer’s disease. This innovative approach offers a promising path forward in the quest for effective treatments for this debilitating condition.

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1. Source: Coherent Market Insights, Public sources, Desk research
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