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While future studies will help confirm the relevance of many of these findings in the mammalian brain, these results reinforce the notion that KBs have a broad array of non-metabolic biological effects that directly impinge on neurotransmission and neuronal excitability (Figure 1)

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In a previous work a significant pathological cupping of the heads of the optic nerve, as a consequence of loss of astrocytes and nerve fibers, was observed

The accumulation of TMAO is a potential irritant to mitochondrial dysfunction

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