Experts from the Center for Advanced Scientific Research at the CUNY Graduate Center, in the United States, have discovered the mechanism responsible for linking cellular stress in the brain to the progression of Alzheimer’s disease.
A microgliathe brain’s primary immune cells, is known to be a causal cell type in Alzheimer’s disease, but it plays a dual role: if some protect brain health, others worsen neurodegeneration.
Pinar Ayata’s team, a researcher and professor in the CUNY ASRC Neuroscience Initiative and the Biology and Biochemistry programs at the CUNY Graduate Center, focused on understanding the functional differences between these microglial populations.
In the most recent study, scientists were able to identify “a new phenotype of neurodegenerative microglia in Alzheimer’s disease, characterized by a signaling pathway related to stress”, highlighted the specialist, cited by .
The team discovered that the activation of this stress pathwayknown as the integrated stress response (ISR), leads microglia to produce and release toxic lipids. In turn, these lipids damage neurons and oligodendrocyte progenitor cells – two types of cells essential for brain function and greatly impacted in this disease.
The good news is that, in preclinical models, blocking this stress response or the lipid synthesis pathway reversed the symptoms do Alzheimer.
“Our findings reveal a link between cellular stress and the neurotoxic effects of microglia in Alzheimer’s disease,” said study co-author Anna Flury. “Directing this path can open new avenues for treatmentstopping the production of toxic lipids or preventing the activation of harmful microglial phenotypes.”
The discoveries are of such magnitude that they could pave the way for the development of new drugs capable of targeting specific microglial populations or their stress-induced mechanisms.
“Potential treatments could significantly slow or even reverse progression of the disease, offering hope to millions of patients and families”, highlighted researcher Leen Aljayousi.
The was published this month in Neuron.
