Cyclic E2 and P4 on Alzheimer’s Disease Pathways

Teresa S Wiley,Jason T Haraldsen

doi:10.4236/aad.2017.61003

Abstract

In recent years, Alzheimer’s disease has been clearly linked to the degradation of microtubules and microtubule-associated tau (τ) and β-amyloid (βA) proteins. Through an examination and evaluation of current literature, we assess the possible effects of the steroid hormones on τ hyperphosphorylation and the regulation of βA proteins and their influence on Alzheimer’s dementia and memory loss. We present a mechanism by which Alzheimer’s cases may be reduced or perhaps even prevented through the use of non-synthetic, steroid hormones prescribed in a cyclic dosing schedule that mimics the rhythmic, escalating and descending production normally observed in a reproductive female body. Given the ability of estrogen to prevent τ hyperphosphorylation and increase metabolism of the βA precursor protein, we propose the possibility of controlling both protein cycles through the exogenous application of estrogen and progesterone may help those patients with active disease as well as prevent the onset of Alzheimer’s and other neurodegenerative diseases.

Highlights

Dementia is a chronic and persistent mental disorder that is typically marked by diminished memory, personality changes, and impaired reasoning [1]
A common form of the disease associated with dementia is Alzheimer’s disease (AD), which is characterized by neuronal cell loss, amyloid plagues, and vascular damage caused by plaque deposition [2] [3] [4] [5]
We review the literature on the τ and βA proteins and their breakdown, examine current treatments that look to only mask the symptoms, and introduce the idea that steroid hormones may provide a pathway to slowing down and possibly halting the progression of this disease

Summary

Introduction

Dementia is a chronic and persistent mental disorder that is typically marked by diminished memory, personality changes, and impaired reasoning [1]. A common form of the disease associated with dementia is Alzheimer’s disease (AD), which is characterized by neuronal cell loss, amyloid plagues, and vascular damage caused by plaque deposition [2] [3] [4] [5] While all these factors can describe AD, the underlying cause remains an unknown. The various interactions and biomechanisms remain elusive To understand this further, we review the literature on the τ and βA proteins and their breakdown, examine current treatments that look to only mask the symptoms, and introduce the idea that steroid hormones may provide a pathway to slowing down and possibly halting the progression of this disease

Current Treatments

The τ Hyperphosphorylation and β-Amyloid Plaques

Effects of Steroid Hormones on Protein Expression

Conclusions