Abstract

In this review, I evaluate emerging evidence regarding the etiology and treatment of Alzheimer’s disease (AD), focusing on the limitations of the amyloid hypothesis and proposing a shift toward a framework centered on cholinergic failure. I argue that this failure results from an inflammation-induced cascade contributed to by infectious exposures (specifically HSV and VZV), potential toxic exposures exacerbated by genetic predisposition, and various lifestyle factors. Utilizing RNA-seq analysis of datasets from the Gene Expression Omnibus and ethically sourced liver tissue, I assess detoxification gene expression and its role in managing environmental stressors. I contend that the convergence of these factors culminates in a failure to maintain adequate levels of Nerve Growth Factor (NGF), resulting in the loss of viability of cholinergic nerves in the brain. Furthermore, I discuss risk assessment and stratification and provide options for risk management through targeted interventions. I prioritize cholinergic intervention and infectious control, followed by lifestyle and detoxification considerations, and discuss the potential of acetylcholinesterase inhibitors (AChEIs) in supporting neuronal survival.

Keywords

growth factor