What role does Tau protein play in Alzheimer’s and other brain diseases?

I’m going to delve into the reason for neurodegenerative diseases, such as Alzheimer’s disease, based on the scientific paper I wrote with Canadian scientist Henry Oh, head of the department of health at the Faculty of Technology, State University of Idaho (USA), published August 13 in the scientific journal Cognitions Scientific, member Journal of the GPJ in the United States.

Tau proteins, an alternative splicing product (a process by which exons of a primary transcript are cleaved at different locations in the newly synthesized RNA molecule) of a single gene, are abundant in central nervous system neurons and are responsible for the stability of microtubules ( protein structures that are part of the cytoskeleton and are formed by the polymerization of the proteins tubulin and almetralopine). When they have a defect, they do not stabilize the microtubules well, leading to dementia.

According to the World Health Organization, more than 35 million people worldwide have Alzheimer’s disease (credits: Bencemor/Shutterstock)

The presence of Aβ (Beta-amyloid) leads neurons to hyperphosphorylate the microtubule binding protein Tau and this increased level redistributes Tau within the axon to dendrites and cell body generating clusters; this process will result in neuronal dysfunction or death leading to neurodegenerative diseases.

Plaques, abnormal deposits of protein fragments, clump together between neurons that contain a neurofibrillary tangle formed by twisted strands of another protein. These plaques are formed when pieces of protein called beta-amyloid clump together, and being chemically “sticky” come together and form plaques. The small clusters block signaling between neurons at synapses and can activate immune system cells causing inflammation and devouring deficient cells.

GSK-3 is a proline-directed serine-threonine kinase that was initially identified as a phosphorylating and inactivating agent of glycogen synthase. Two isoforms, alpha and beta, show a high degree of amino acid homology. GSK-3-Beta is involved in energy metabolism, neuronal cell development and body pattern formation. GSK-3 has been the subject of research as it is linked to a number of diseases including type 2 diabetes, Alzheimer’s disease, inflammation, cancer and bipolar disorder.

Knowing these mechanisms, some studies have found a neuroprotective effect of the mineral lithium — present in grains, beef, eggs and vegetables — inhibiting the GSK-3-Beta enzyme, which plays an important role in the degeneration of neurons. Suggesting that the inhibition of the activity of GSK-3-Beta with chronic treatment with lithium in hippocampal neurons obtaining an opposite effect in cortical neurons and without alterations in the Tau protein.

ARTICLE Cognitionis: https://doi.org/10.38087/2595.8801.90

Fabiano de Abreu Rodrigues, columnist of TechWorld, holds a doctorate and master’s degree in Health Sciences in the areas of Neuroscience and Psychology, specializing in Electrical Properties of Neurons (Harvard), programming in Python at USP and in Artificial Intelligence at IBM. He is a member of Mensa International, the association of the smartest people in the world, the Portuguese and Brazilian Society of Neuroscience and the European Federation of Neuroscience. He is director of the Heraclitus Research and Analysis Center (CPAH), considered one of the main national scientists for intelligence and high IQ studies

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