This week media stories have surfaced that a diet of plant sugar will deal with progressive MS because it rejuvenates the microglia to clear nerve debris away to promote recovery. Great we say. This study identifies a trigger factor called ATG7 . The Autophagy related 7 protein acts as an essential protein for cell degradation and its recycling. But we know this already based on loads of studies from Cambridge and we say NSS.
The Cambrdige diet to rejuvenate the microglia involves the use of metforin and I say watch this space for trials, but should we be comparing with the Stockholm diet of Trehalose (a sugar containing two glucose molecules) that acts on ATG7 to rejuvenate the microglia. Loss of ATG7 in Fruit flies and Mice is related to nerve loss so stimulation of the pathway may save nerves.
Is this what could occur in progressive MS, maybe but the experiment are most relevant to how you recover form a relapse. As ProfG suggested it indicates that mocroglial can be good guys.
Trehalose is only 50% as sweet as table sugar, and does not increase blood sugar or levels nearly as much as the same dose of regular sugar. Side Effects include bloating and diarrhea. Decreasing dosage will prevent these discomforts.
Berglund et al. Microglial autophagy–associated phagocytosis is essential for recovery from neuroinflammation, Science Immunology 16 Oct 2020:Vol. 5, Issue 52, eabb5077.
Multiple sclerosis (MS) is a leading cause of incurable progressive disability in young adults caused by inflammation and neurodegeneration in the central nervous system (CNS). The capacity of microglia to clear tissue debris is essential for maintaining and restoring CNS homeostasis. This capacity diminishes with age, and age strongly associates with MS disease progression, although the underlying mechanisms are still largely elusive. Here, we demonstrate that the recovery from CNS inflammation in a murine model of MS is dependent on the ability of microglia to clear tissue debris. Microglia-specific deletion of the autophagy regulator Atg7, but not the canonical macroautophagy protein Ulk1, led to increased intracellular accumulation of phagocytosed myelin and progressive MS-like disease. This impairment correlated with a microglial phenotype previously associated with neurodegenerative pathologies. Moreover, Atg7-deficient microglia showed notable transcriptional and functional similarities to microglia from aged wild-type mice that were also unable to clear myelin and recover from disease. In contrast, induction of autophagy in aged mice using the disaccharide trehalose found in plants and fungi led to functional myelin clearance and disease remission. Our results demonstrate that a noncanonical form of autophagy in microglia is responsible for myelin degradation and clearance leading to recovery from MS-like disease and that boosting this process has a therapeutic potential for age-related neuroinflammatory conditions.