Researchers reveal glycogen breakdown could fight Alzheimer’s damage

Recent research published in the journal Nature Metabolism highlights a groundbreaking discovery about glycogen, the food storage form of glucose in the brain, and its potential role in addressing Alzheimer's disease. This research, centering on experiments conducted with genetically modified fruit flies representing tauopathy—a condition linked to tau protein buildup—illustrates how impaired glycogen breakdown may contribute to neurodegeneration associated with Alzheimer's. The research team utilized not only the fly models but also human cell models sourced from patients affected by tau mutations, along with postmortem brain samples from individuals diagnosed with Alzheimer's or related neurodegenerative diseases. In both experimental setups, there's a notable rise in glycogen levels observed alongside an impairment in glycogen breakdown. The findings suggest that tau proteins, which accumulate in Alzheimer's, interfere with glycogen metabolism, leading to diminished neuronal health and an increased risk of cell damage. Additionally, this study examined the effects of dietary restrictions on the brain health of the fruit flies. Remarkably, restricted diets corresponded with increased glycogen breakdown, shedding light on how nutritional factors may influence neurodegenerative processes. The research led to the identification of a special molecule, 8-Br-cAMP, which mimics the antioxidant protective effects seen with dietary restriction. While preliminary, these findings pave the way for potential dietary or pharmacological avenues to slow the progression of Alzheimer's and similar conditions. It was emphasized that current data is based on animal and human cell models, and the ultimate effectiveness and safety in live human patients remain untested and uncertain. Furthermore, unanswered questions linger regarding the exact role of glycogen in Alzheimer's disease, specifically whether it acts as a contributor to the pathology or merely as a byproduct of neural damage. Overall, while the results show promise, researchers like Kapahi and Okun are pragmatic about the need for further research, emphasizing that their work is still in its early stages and warrants cautious optimism. They stress the importance of continuing explorations into how neuronal health can be sustained, especially in the face of prevalent neurodegenerative diseases like Alzheimer's, which currently affect over seven million people in the U.S. alone.