Alzheimer's disease (AD) as a disorder of the plasma membrane

Walter J Lukiw

doi:10.3389/fphys.2013.00024

Abstract

GENERAL COMMENTARY article Front. Physiol., 15 February 2013Sec. Membrane Physiology and Membrane Biophysics https://doi.org/10.3389/fphys.2013.00024

Highlights

Alzheimer’s disease (AD) is a common, progressive degeneration of human brain structure and function, resulting in a deterioration of mood, behavior, functional ability, cognition, and memory (Alzheimer et al, 1995)
Besides the appearance of neurofibrillary tangles, at the root of the AD problem appears to be an up-regulation in the generation of small, toxic, and highly amyloidogenic 42 amino acid amyloid beta (Aβ42) peptides that self-associate, clumping into pro-inflammatory and microglia-activating senile plaques (SP)
Dietary and systemic factors such as cholesterol, which perturb the biophysical structure of the phospholipid membrane and reorganize lipid raft domains where βAPP processing appears to occur, further contributes, via protein-lipid and protein-protein interactions, to membrane-mediated dysfunction of homeostatic βAPP neurobiology (Hicks et al, 2012; Kania et al, 2012)

Summary

Introduction

Alzheimer’s disease (AD) is a common, progressive degeneration of human brain structure and function, resulting in a deterioration of mood, behavior, functional ability, cognition, and memory (Alzheimer et al, 1995). Dietary and systemic factors such as cholesterol, which perturb the biophysical structure of the phospholipid membrane and reorganize lipid raft domains where βAPP processing appears to occur, further contributes, via protein-lipid and protein-protein interactions, to membrane-mediated dysfunction of homeostatic βAPP neurobiology (Hicks et al, 2012; Kania et al, 2012).

Results

Conclusion