Muscle-building complement may help protect memory and stop Alzheimer’s disease

Muscle-building complement may help protect memory and stop Alzheimer’s disease

The key to protecting your memory could also be a staple of a bodybuilder’s weight-reduction plan. RUSH researchers recently discovered that a muscle-building complement called beta-hydroxy beta-methylbutyrate, also called HMB, may help protect memory, reduce plaques and ultimately help prevent the progression of Alzheimer’s disease.

HMB is just not a prescription drug or a steroid, but an over-the-counter complement that is offered in sports and fitness stores. Bodybuilders commonly use HMB to extend exercise-induced gains in muscle size and strength while improving exercise performance. HMB is taken into account secure even after long-term use, with no known unintended effects.

“This may occasionally be certainly one of the safest and the simplest approaches to halt disease progression and protect memory in Alzheimer’s disease patients,” said Kalipada Pahan, PhD, the Floyd A. Davis, MD, Professor of Neurology and professor of neurological sciences, biochemistry and pharmacology at RUSH Medical College.

Studies in mice with Alzheimer’s disease have shown that HMB successfully reduces plaques and increases aspects for neuronal growth to guard learning and memory, in keeping with neurological researchers at RUSH.

“Understanding how the disease works is vital to developing effective drugs to guard the brain and stop the progression of Alzheimer’s disease,” Pahan said.

Previous studies indicate that a family of proteins often known as neurotrophic aspects are drastically decreased within the brains of individuals with Alzheimer’s disease and have been found to assist in survival and performance of neurons, that are cells that receive and send messages from the body to the brain and vice versa.

“Our study found that after oral consumption, HMB enters into the brain to extend these useful proteins, restore neuronal connections and improve memory and learning in mice with Alzheimer’s-like pathology, akin to plaques and tangles,” Pahan said.

The study findings indicate that HMB stimulates a nuclear hormone receptor called PPARα throughout the brain that regulates the transport of fatty acids, which is vital to the success of HMB as a neuroprotective complement.

“If mouse results with HMB are replicated in Alzheimer’s disease patients, it will open up a promising avenue of treatment of this devastating neurodegenerative disease,” Pahan said.

Alzheimer’s disease is an irreversible, progressive brain disease that slowly destroys memory and pondering skills and, eventually, even the power to perform the only tasks. In most individuals with Alzheimer’s, symptoms first appear after age 60. Alzheimer’s disease is probably the most common reason behind dementia amongst older people, affecting as many as 6 million Americans and greater than 10% of individuals age 65 and older. About two-thirds of Americans with Alzheimer’s disease are women.

Results from the study, funded by the National Institutes of Health, were recently published within the Cell Reports.

Other RUSH researchers involved on this study are Ramesh K. Paidi, PhD, Sumita Raha, PhD, and Avik Roy, PhD.