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Alzheimer’s disease (AD) is a complex cognitive disorder for which the single greatest risk factor is age. The pathophysiological basis for AD is still a matter of debate with no current hypothesis explaining all of the complex pathological changes observed. These include neurofibrillary tangles, amyloid plaques, neuroinflammation, hypomyelination, neuronal shrinkage (eg. Nbasalis cholinergic neurons, resulting in a dramatic cholinergic deficit), ocular pathology, microvascular pathology and liver peroxisomal dysfunction. The hypothesis that we are presenting, namely peroxisomal dysfunction resulting in decreased supply of critical ethanolamine plasmalogens to the brain, eye and vascular endothelium, is the first hypothesis that can potentially explain all of these complex pathologies in AD. The value of this hypothesis is that it is imminently testable via resupply of critical ether lipid precursors of plasmalogens. PPI-1011 is such a drug candidate and will be presented after a review of the basis of this hypothesis.

Plasmalogen Deficit: A New and Testable Hypothesis for the Etiology of Alzheimer’s Disease