This stuff in the gut may contribute to Alzheimer’s disease

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In a new study, researchers found that misfolded protein build-up in the gut may contribute to the development of Alzheimer’s-like symptoms.

This could suggest a new treatment approach for Alzheimer’s disease that would target the gut before symptoms of cognitive deficits appear in patients.

The research was conducted by a team at The Chinese University of Hong Kong.

The misfolded protein, known to be involved in Alzheimer’s disease, called beta-amyloid, was injected into the guts of mice and traveled to the “gut-brain” (the nervous system in our gut), and also to the brain.

The team found if some of the beta-amyloid build up in the central nervous system (brain and spinal cord) is originating from the outside the brain (peripheral nervous system), reducing the amount that makes it to the brain, or trapping the protein in the periphery may delay the onset of Alzheimer’s disease.

This treatment would begin before any signs of dementia appear in the patient.

In the study, the researchers injected fluorescently-tagged beta-amyloid into the gut of mice. The proteins moved to the nervous system in our 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 our brain that affects our memory. These animals experienced cognitive impairments.

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.

Development of drug treatments for Alzheimer’s disease has been unsuccessful so researchers instead need new approaches for preventing AD development.

This could be a potential route for preventing the disease by targeting these misfolded proteins in the gut.

The team says this concept is similar to the transport of misfolded proteins from the gut such as those responsible for mad cow disease.

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.

One author of the study is John A Rudd.

The study is published in the Journal of Physiology.

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