For example, acetate supplementation appears to ameliorate inflammatory and neurodegenerative damage in preclinical models that do not develop amyloidosis or tauopathy, as in models of sleep disruption,19 Coffin-Siris syndrome20 and multiple sclerosis21 but can exacerbate the same phenomena in models that have amyloid and tau deposition.5,6 Although the causal link between SCFAs and cognitive impairment is far from being proven, these results strengthen the hypothesis that SCFAs have distinct effects and mechanisms of action depending on the disease. Here, MAPT is linked to amyloidosis.