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Diagnostic workup was notable for thiamine deficiency, NCS/EMG showing a severe, axonal polyneuropathy, and nerve biopsy redemonstrating severe axonal neuropathy

Annals of the New York Academy of Sciences (2010) Crockford D Annals of the New York Academy of Sciences (2007)

Thus, our data suggest that neuronal dysfunction in early AD largely depends on the continuous de novo release of (nascent) A monomers, which immediately start forming toxic oligomers or aggregates, rather than a stable pool of such A species

Mitophagy, a key component of MQC, is impaired in the hippocampus of AD patients [107]

-(as pyridoxal-5'-phosphate)

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