Targeting Alzheimer’s Pathology may Offer Treatment for ALS

New insights on ALS points to a potentially promising treatment strategy where blocking tau molecules may render benefits to ALS patients.

New insights on ALS (Amyotrophic Lateral Sclerosis) point to a potentially promising treatment strategy where blocking tau molecules (hallmark of Alzheimer’s disease) may render benefits to ALS patients as per a study at the Massachusetts General Hospital, published in Molecular Neurobiology.

ALS is a degenerative condition where the brain and spinal cord nerve cells are attacked progressively, thereby affecting the individuals’ ability to move, speak, eat, and even breathe. Although ALS has no cure, earlier studies have implicated that mitochondrial dysfunction (generate energy within cells) plays an important role in the development of ALS.

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‘New insights on ALS (Amyotrophic Lateral Sclerosis) point to a potentially promising treatment strategy where blocking tau molecules (hallmark of Alzheimer’s disease) may render benefits to ALS patients. ’

Previous studies have also linked changes in mitochondrial function to interactions between an abnormal form of tau which accumulates in the brains of patients within Alzheimer’s disease, and a mitochondrial protein called dynamin-related protein 1 (DRP1).

The present study thereby provides a better understanding of the mechanisms behind the development of amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, by piecing these bits of information together and thus points to a potential treatment strategy.

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Hence, the team examined whether interactions between this abnormal tau with DRP1 might also promote mitochondrial dysfunction in ALS and whether reducing tau could be a novel and promising therapeutic approach to fight the disease.

It was found that the abnormal form of tau is present in brain tissue of ALS patients, and is located where tau is not normally found and interacts with DRP1.

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The cells’ mitochondria fragmented and oxidative stress also increased when these ALS brain tissues with abnormal tau were grown in contact. Importantly, reducing tau with a specific degrader reversed these effects, reducing mitochondrial fragmentation and lowering oxidative stress.

“We demonstrated for the first time that targeting tau with a new class of small molecules that selectively degrade it can reverse the ALS-induced changes in mitochondria’s shape and function, highlighting tau as a potential therapeutic target,” says, Ghazaleh Sadri-Vakili, Ph.D., director of the NeuroEpigenetics Laboratory at the MassGeneral Institute for Neurodegenerative Disease and the Healey Center for ALS at MGH.

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Source-Medindia