New study sheds light on how Alzheimer’s tau tangles begin

Inhibition of GCPII lowers pT217Tau in the brains of aged macaques.

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A recent study conducted by researchers from Yale School of Medicine and Johns Hopkins University has made significant progress in understanding the underlying causes of Alzheimer’s disease. The study delves into the origins of tau protein tangles, which are known to damage neurons in the brains of individuals with Alzheimer’s.

Researchers have found that an experimental drug can help reduce the harmful changes in tau proteins that damage neurons in Alzheimer’s disease. While much Alzheimer’s research has focused on amyloid plaques, this study is about slowing down the damage in a tau molecule, which can lead to tangles and brain cell degeneration.

Senior author Amy Arnsten, the Albert E. Kent Professor of Neuroscience at Yale School of Medicine and professor of neurobiology and psychology in Yale’s Faculty of Arts and Sciences, said, “We were able to reduce the phosphorylation of tau by restoring regulatory actions that are lost with age and inflammation. The mechanism of protection is different from other approaches undertaken so far.”

The study was published in a journal called Alzheimer’s & Dementia TRCI.

In their research, researchers in Arnsten’s lab wanted to find ways to reduce a harmful process in Alzheimer’s disease before it causes damage to brain cells. They focused on a brain enzyme called GCPll that’s linked to inflammation. This enzyme weakens the protective effects of a receptor on brain cells called mGluR3, which helps with thinking. The researchers discovered that a drug that blocks GCPll, called 2-MPPA, reduced this harmful process in older monkeys with tau brain problems.

The aim is to create a drug that people can take. Barbara Slusher, a co-author of the study, said, “We want to make a GCPll blocker safe for humans to take by mouth. We think this could be helpful.”

In conclusion, this research offers valuable insights into the mechanisms of Alzheimer’s disease, emphasizing the importance of tau proteins and their phosphorylation in neurological damage. The hope is to translate these findings into developing safe and effective treatments for this devastating disease.

Journal reference:

  1. Shveta Bathla, Dibyadeep Datta, et al., Chronic GCPII (glutamate-carboxypeptidase-II) inhibition reduces pT217Tau levels in the entorhinal and dorsolateral prefrontal cortices of aged macaques. Alzheimer’s & Dementia TRCI. DOI: 10.1002/trc2.12431.

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