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Researchers cartel protein gene interactions involved in Alzheimer's disease



BYLD

BYLD: In the brain, due to the disease of Alzheimer's, abnormal levels of the beta-amyloid protein coincided with each other to form plaques (seen in brown) that they collect between neurons and the function of a cell disorder . Abnormal collections …
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Credit: National Institute for Aging, NIH

Under the amazing challenges of diagnosing and treating Alzheimer's disease (AD), patients with asymptomatic and symptomatic versions of degenerative states may share similar neuropathological disorders, but experience significantly different rates of cognitive decline.

In a new study, July 23, 2019 published Cell report, a team led by researchers from the University of California San Diego School of Medicine used the transcriptome – the sum of all messenger RNA (mRNA) molecules expressed from genes – to examine 414 participants with clinically diagnosed and neuropathologically confirmed AD with a age-matched, non-demented control group from a community-based neuropathological study.

Their findings suggest that protein interaction integration with gene reproductions can generate a wide range for characterizing changes in the molecular network related to AD.

While familial AD has a strong genetic factor, the causes of sporadic AD (the most common form) are multiple and not fully known. Primary risk factors include age, gender and family history, but also include a variety of biological, psychological and social factors.

Many research has focused on two major elements of AD pathology – the accumulation of amyloid protein plaques and abnormal neurofibrillary tau proteins tangles in the brain, which are thought to cause neuronal dysfunction and death. But scientists increasingly recognize the relevance and importance of other factors, such as inflammation, blood circulation problems, and harrode atrophy – all correlate with clinical symptoms of cognitive decline and have led to changes in diagnostic criteria in recent decades, "wrote the authors.

The new study combined analyzes of gene perturbations and protein interactions, said senior author Robert Rissman, PhD, professor of neurosciences at UC San Diego School of Medicine, director of a Biomarker Core for Alzheimer's Disease Cooperative Study (ADCS) and director of & # 39; a Neuropathology / Brain Bank and Biomarker Cores for the UC San Diego Shiley-Marcos Alzheimer's Disease Research Center, which identified ultimately functionally distinguished assembled clusters of genes, offering extensive changes in expression levels in AD . These clusters corresponded broadly with synaptic transmission, metabolism, cell cycle, cell survival and immune response – all critical aspects involved in AD pathology.

"One of the major problems in AD research is identifying patients at risk at the right time," Rissman said. "Understanding the gene networks that can change into specific patient groups can help streamline clinical trial recruitment and reduce cost and time for files. With the field more and more toward pre-symptomatic disease, we must our understanding of molecular expansion mechanisms underlying the entire spectrum of diseases. "

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May authors embrace: Saranya Canchi, UC San Diego and Veterans Affairs San Diego Healthcare System; Balaji Raao, Deborah Masliah, Sara Brin Rosenthal, Roman Sasik and Kathleen M. Fisch, all at UC San Diego; Philip L. De Jager, Columbia University Medical Center; and David A. Bennett, Rush University Medical Center.

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