Hong Kong, July 5
Misfolded protein build-up in the gut could contribute to the development of Alzheimer’s-like symptoms, researchers have shown.
This new finding, published in the Journal of Physiology, suggests a new treatment approach for Alzheimer’s disease that would target the gut before symptoms of cognitive deficits appear in patients.
“As these proteins were found in the gut, this suggests environmental factors might be contributing to cognitive deficits seen in Alzheimer’s disease and other conditions,” the researchers from the Chinese University of Hong Kong, wrote.
Beta-amyloid, the misfolded protein known to be involved in Alzheimer’s disease, was injected into the guts of mice and travelled to the “gut-brain” (the nervous system in the gut), and also to the brain.
The proteins moved to the nervous system in the gut.
The misfolded proteins were seen a year later in parts of the brain involved in cognitive deficits of Alzheimer’s disease including the hippocampus, the part of the brain that affects the memory.
According to the researchers, these animals experienced cognitive impairment.
As this study was conducted in mice, it needs verification by looking for post-mortem changes in inflammation in the gut and brain of patients with Alzheimer’s disease, the research team noted.
“This concept is similar to the transport of misfolded proteins from the gut such as those responsible for mad cow disease,” said study senior author John A. Rudd.
“If this is the case, a similar process may start in humans many years ahead of the manifestations of the classical hallmarks of AD including memory loss, and so prevention strategies would need to start earlier as well,” he added.
“Development of drug treatments for Alzheimer’s disease has been unsuccessful so we instead need new approaches for preventing AD development,” the study authors wrote. “This could be a potential route for preventing the disease by targeting these misfolded proteins in the gut,” they noted.
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(This story has not been edited by BDC staff and is auto-generated from a syndicated feed from IANS.)
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