Basic research into neurodegenerative disorders, like Alzheimer’s disease, is heavily focused on understanding genetic susceptibility and biochemical triggers of pathology, as well as disturbances to the intrinsic electrophysiological properties of affected neurons. Often overlooked is the role of mechanics, particularly mechanical properties and mechano‑sensitivity/‑responsiveness of neurons and glia. Recent evidence confirms that mechanical signals regulate CNS development and pathophysiology. In this talk, I will discuss the role of mechanics in both physiological and pathophysiological brain ageing. A defining pathophysiological hallmark of Alzheimer’s disease is the amyloid plaque; an extracellular deposit of aggregated fibrillar Aβ1‑42 peptides. Amyloid plaques are hard, brittle structures scattered throughout the hippocampus and cerebral cortex and are thought to cause hyperphosphorylation of tau, neurofibrillary tangles, and progressive neurodegeneration. Glia are highly mechanosensitive cells and can sense the mismatch between the normally soft mechanical environment of the brain and very stiff amyloid plaques via mechanosensing ion channels. Both ageing and peripheral infection augment amyloid plaque‑induced upregulation of mechanoresponsive ion channels in astrocytes. Further research is required to investigate whether modulating mechanically-gated channel opening will protect or exacerbate the disease state, and most importantly, if they are novel drug targets for age‑related dementia
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