A study led by researchers at the City University of New York (CUNY) has uncovered a critical mechanism behind Alzheimer’s disease involving the integrated stress response (ISR) pathway.
 
Blocking this pathway in mouse models prevented synapse damage and reduced the buildup of tau proteins—hallmarks of Alzheimer's disease, as reported by the website science alert.

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Microglia turn harmful under stress

The researchers discovered that the ISR pathway causes brain immune cells called microglia to become dark and harmful, rather than protective. 

These stressed microglia release damaging lipids that contribute to synapse destruction and disrupt neuronal communication. 

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The team found around twice as many stressed microglia in Alzheimer’s-affected brains compared to healthy ones. 

Targeting the ISR pathway for treatment

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The study suggests that targeting the ISR pathway could offer new treatment strategies for Alzheimer's. 

"These findings reveal a critical link between cellular stress and the neurotoxic effects of microglia in Alzheimer's disease," said Anna Flury, a molecular biologist at CUNY. 

"Targeting this pathway may open up new avenues for treatment by either halting the toxic lipid production or preventing the activation of harmful microglial phenotypes," she added. 

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Misfolded proteins, which are commonly linked to dementia, might trigger the ISR, meaning the stress signals both result from and accelerate Alzheimer's progression.

Potential for slowing Alzheimer's disease

By halting the toxic effects of the ISR pathway, scientists could slow Alzheimer’s progression. 
Neuroscientist Leen Aljayousi, from CUNY, says, "Such treatments could significantly slow or even reverse the progression of Alzheimer's disease, offering hope to millions of patients and their families." 

These findings provide valuable insight into the neurodegenerative process and highlight the potential for developing treatments that target the harmful activation of microglia.

(With inputs from agencies)