Summary: Researchers have discovered that the Tau proteins, usually linked to neurological disorders like Alzheimer’s, even has a protective function in the mind. Tau assists in the release of fat droplets in cortical cells, which store toxic lipids and protect neurons, to combat oxidative stress.
But, when Tau is mutated or excluded, this protective mechanism fails, leading to increased mental harm. By utilizing Tau’s defensive abilities, this finding may open new avenues for treating neurological conditions.
Important Information:
- Tau reduces neuronal oxidative stress by forming fat particles in glial tissue.
- Tau’s protecting role is hindered by mutations, which are a cause of degenerative diseases.
- This finding points to novel cure options that emphasize Tau’s safe effects.
Origin: Baylor College of Medicine
A study by researchers at , Baylor College of Medicine , and the , Jan and Dan Duncan Neurological Research Institute , ( Duncan NRI ) at Texas Children’s Hospital, reveals that the protein Tau – a key player implicated in several neurodegenerative conditions including Alzheimer’s disease – also plays a positive role in the brain.
Tau promotes healthy aging by reducing the effects of excessive reactive oxygen species ( ROS ) or free radicals on neuronal damage.
The , review  , was published in , Nature Science.
ROS are the body’s several cellular byproducts, according to Rosie. While lower levels of ROS are beneficial, extra ROS is dangerous to cells as it triggers the production of harmful forms of other molecules that cause oxidative tension, including peroxidated lipids”, said guide author , Dr. Lindsey Goodman, a postdoctoral fellow in the laboratory of , Dr. Hugo Bellen.
” Cells are particularly susceptible to oxidative stress and are destroyed if peroxidated fat levels are not strongly controlled,” says one author.
The brain is protected from reactive harm by fat particles.
Growing evidence points to the idea that our brains have employed a variety of chemopreventive measures to combat ROS-induced oxidative damage.
The Bellen group discovered one of the methods in which neurons export these dangerous peroxidated lipids to nearby glial cells, which sequester them into fat droplets for backup and potential energy production.
Goodman said,” This method effectively removes and neutralizes these dangerous fat.” ” In the current review, we looked into the role that Tau plays in the formation of glial fat droplets.”
The study discovered that systemic regular Tau in flies is necessary for neuronal ROS protection and the formation of glial lipid droplets. Also, Tau was required in parietal tissue obtained from animals and humans to form fat droplets.
When this individual Tau protein had disease-causing mutations and was linked to an increased risk of Alzheimer’s disease, the glia were unable to form fat droplets in response to cerebral ROS, even though the expression of ordinary people Tau was sufficient to stop the formation and maturation of glial fat droplets in flies lacking their own Tau.
According to Goodman,” This argues that mutations in Tau perhaps reduce the protein’s ordinary capacity to prevent oxidative stress and increase its accumulation into the common hallmarks of illness,” as previously stated. Overall, the findings support a novel neurotoxic responsibility for Tau against the toxicology that ROS can play.
Utilizing established fly and mouse models of Tau-mediated conditions that overexpress the disease-causing people Tau proteins in glia, new connections with disease were made. In these circumstances, the researchers once more observed cortical fat droplets and glial cell demise in response to cerebral ROS. This demonstrated that when too much or too little of Tau is harmful, it is a dosage-sensitive cortical fat droplet regulator.
The study opens the door to potential new strategies to decrease, invert, and treat neurological conditions, according to Bellen, related author of the work, by revealing a shocking new neurotoxic role for Tau.
He holds a Chair in Neurogenetics at Duncan NRI and is a recognized company professor at Baylor. Becken is also a Baylor University Professor of Developmental Biology.
In conclusion, this research demonstrates that Tau also plays a” good man” part in glia by preventing oxidative damage, preventing oxidative damage, and thus protecting our brains, as opposed to its typical “bad guy” role in neurological disease. Nevertheless, when Tau is unavailable or when deficient Tau protein are present, this safe effect disappears, leading to illness.
Funding: This work was supported by several grants from the National Institutes of Health, the Canadian Institutes of Health and Research Doctoral Award, Sloan Research Fellowship from the Alfred P. Sloan Foundation, Canada Research Chairs program, a CIHR project grant and a Grant-in-Aid for Scientific Research on Challenging Research ( Exploratory ).
About this study in neurology
Author: Molly Chiu
Source: Baylor College of Medicine
Contact: Molly Chiu – Baylor College of Medicine
Image: The image is credited to Neuroscience News
Original Research: Closed exposure.
Lindsey Goodman and colleagues ‘” Tau is required for neuronal oxidative stress resistance and glial lipid drop creation.” Nature Science
Abstract
For cerebral oxidative stress, glial fat particle formation and resistance are governed by Tau.
A common trait of tauopathies, defined by tau accumulations in neurons and glia, is the accumulation of reactive oxygen species ( ROS). High levels of ROS in neurons result in the production and export of toxic peroxidated lipids ( LPOs ). These LPOs are incorporated into lipid droplets ( LDs ) for storage and catabolism by the glia uptake.
We found that overexpressing Tau in glia affects Mormons in mosquitoes and mouse neuron–astrocyte co-cultures, sensitizing the glia to harmful, cerebral LPOs. Using a new fly , tau , loss-of-function gene and RNA-mediated intervention, we found that systemic Tau is required for cortical LD development and protection against cerebral LPOs.
Similarly, endogenous Tau is required in rat astrocytes and human oligodendrocyte-like cells for LD formation and the breakdown of LPOs.
Behaviorally, flies lacking glial Tau have decreased lifespans and motor defects that are rescuable by administering the antioxidant , N-acetylcysteine amide.
Overall, this study provides insight into the crucial role that Tau plays in brain glia in reducing ROS.
