Scientists Found a Way to Help the Brain Bounce Back From Alzheimer's

Arthur T Knackerbracket writes:

https://scitechdaily.com/scientists-found-a-way-to-help-the-brain-bounce-back-from-alzheimers/

For more than a hundred years, Alzheimer's disease (AD) has been regarded as a condition that cannot be undone. Because of this assumption, most scientific efforts have focused on stopping the disease before it starts or slowing its progression, rather than attempting to restore lost brain function. Despite decades of research and billions of dollars invested, no drug trial for Alzheimer's has ever been designed with the explicit goal of reversing the disease and restoring normal brain performance.

That long-standing belief is now being directly tested by researchers from University Hospitals, Case Western Reserve University, and the Louis Stokes Cleveland VA Medical Center. Their work asked a fundamental question that had rarely been explored: Can brains already damaged by advanced Alzheimer's recover?

The study was led by Kalyani Chaubey, PhD, of the Pieper Laboratory and was published on December 22 in Cell Reports Medicine. By analyzing multiple preclinical mouse models alongside brain tissue from people with Alzheimer's, the researchers identified a critical biological problem underlying the disease. They found that Alzheimer's is strongly driven by the brain's failure to maintain normal levels of a key cellular energy molecule called NAD⁺. Just as important, they showed that keeping NAD⁺ levels in balance can both prevent the disease and, under certain conditions, reverse it.

NAD⁺ naturally declines throughout the body as people age, including in the brain. When this balance is disrupted, cells gradually lose the ability to carry out essential processes needed for normal function and survival. The team found that this loss of NAD⁺ is far more pronounced in the brains of people with Alzheimer's. The same severe decline was also observed in mouse models of the disease.

[...] Amyloid buildup and tau abnormalities are among the earliest and most important features of Alzheimer's. In both mouse models, these mutations led to extensive brain damage that closely resembles the human condition. This included breakdown of the blood-brain barrier, damage to nerve fibers, chronic inflammation, reduced formation of new neurons in the hippocampus, weakened communication between brain cells, and widespread oxidative damage. The mice also developed severe memory and thinking problems similar to those experienced by people with Alzheimer's.

After confirming that NAD⁺ levels drop sharply in both human and mouse Alzheimer's brains, the researchers explored two different strategies. They tested whether preserving NAD⁺ balance before symptoms appear could prevent Alzheimer's, and whether restoring NAD⁺ balance after the disease was already well established could reverse it.

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