Friday, October 22, 2021

Metabolism modulates network synchrony in the aging brain

Wow, this work from Weistuch et al. temps me to reconsider my decision to stay away from the various mitochondrial metabolism stimulating supplements I have experimented with over the past 10-15 years (they made me a bit hyper). It has been hypothesized that declining glucose metabolism in older brains drives the loss of high-cost (integrated) functional activities (activities of the sort I'm trying to carry out at the moment in cobbling together a coherent lecture from diverse sources). From the paper's introduction:
We draw on two types of experimental evidence. First, as established using positron emission tomography, older brains show reduced glucose metabolism. Second, as established by functional MRI (fMRI), aging is associated with weakened functional connectivity (FC; i.e., reduced communication [on average] between brain regions). Combining both observations suggests that impaired glucose metabolism may underlie changes in FC. Supporting this link are studies showing disruptions similar to those seen with aging in type 2 diabetic subjects.

The Significance Statement and Abstract:  

Significance

How do brains adapt to changing resource constraints? This is particularly relevant in the aging brain, for which the ability of neurons to utilize their primary energy source, glucose, is diminished. Through experiments and modeling, we find that changes to brain activity patterns with age can be understood in terms of decreasing metabolic activity. Specifically, we find that older brains approach a critical point in our model, enabling small changes in metabolic activity to give rise to an abrupt reconfiguration of functional brain networks.
Abstract
Brain aging is associated with hypometabolism and global changes in functional connectivity. Using functional MRI (fMRI), we show that network synchrony, a collective property of brain activity, decreases with age. Applying quantitative methods from statistical physics, we provide a generative (Ising) model for these changes as a function of the average communication strength between brain regions. We find that older brains are closer to a critical point of this communication strength, in which even small changes in metabolism lead to abrupt changes in network synchrony. Finally, by experimentally modulating metabolic activity in younger adults, we show how metabolism alone—independent of other changes associated with aging—can provide a plausible candidate mechanism for marked reorganization of brain network topology.

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