Abstract
Alzheimer’s disease represents a major healthcare problem, with over five million Americans estimated to suffer from this disease, and a recent study showing that AD has now become the third leading cause of death, trailing only cardiovascular disease and neoplasia [1]. The cause(s) of AD remain incompletely determined, and there is currently no truly effective treatment. However, accumulating data suggest important contributions from metabolic abnormalities such as insulin resistance, metabolic syndrome, chronic inflammation, hypovitaminosis D, hormonal deficiencies, and hyperhomocysteinemia, among others [2]. Despite this, most clinical evaluations of patients with cognitive decline do not include extensive metabolic or genomic evaluations. Furthermore, given Research Paper the perceived poor prognosis for AD, in patients with evidence of amyloid-β accumulation by amyloid PET imaging or, indirectly, by cerebrospinal fluid profile, there has been little incentive to perform extensive evaluations of hormonal status, nutritional status, toxicity status, metal status, gastrointestinal permeability, or other laboratory evaluations perceived by healthcare systems as “non-standard.” However, studies such as the recent FINGER study [3] suggest that metabolic factors may play important roles in the neurodegenerative process, at least early in the pathogenetic process. Recent results from the evaluation of neural exosomes and nanosomes support the notion that metabolic abnormalities are present in patients with cognitive decline, often years prior to diagnosis of AD [4]. Therefore, it may be productive, both from the standpoint of identifying novel biomarkers and from the standpoint of identifying treatable metabolic abnormalities, to perform metabolic profiling of patients with cognitive decline and those at risk for such decline.