Endogenous glucocorticoids: role in the etiopathogenesis of Alzheimer's disease

Research output: Contribution to journalReview article

Abstract

Endogenous glucocorticoids (eGCs) are steroid hormones with a wide spectrum of physiological effects. However, enhanced basal eGCs levels have been observed in patients affected by Alzheimer's disease (AD) and they have been correlated with dysregulation of the hypothalamic-pituitary-adrenocortical axis, hippocampal degeneration and reduced cognitive/memory performance. Therefore, it has been proposed that elevated concentration of eGCs might have a role in AD pathogenesis. AD is the most common form of dementia, characterized by the pathological accumulation of two proteins: the Amyloid Beta (Aβ) and the microtubule-associated protein tau in the neurons of the hippocampus and prefrontal cortex. In particular, the hippocampus, the cerebral area involved in learning and memory, is the brain region more vulnerable to chronic eGCs exposure. Although clinical studies have failed to establish a direct causative link between eGCs e and AD pathogenesis, evidences from pre-clinical studies have shown that increased eGCs levels accelerate the formation of Aβ in AD animal models by promoting the amyloidogenic pathway, and in parallel by reducing Aβ clearance, through transcriptional mechanisms involving the Glucocorticoid receptors. Instead, the effects of stress on tau phosphorylation seem to be mainly mediated bv the corticotropin-releasing factor receptor (CRFR1) and independent from stress-induced eGCs elevation.

Original languageEnglish
Pages (from-to)1-12
Number of pages12
JournalNeuroendocrinology Letters
Volume38
Issue number1
Publication statusPublished - Feb 2017

Fingerprint

Glucocorticoids
Alzheimer Disease
Hippocampus
Corticotropin-Releasing Hormone Receptors
Serum Amyloid A Protein
Microtubule-Associated Proteins
Amyloid beta-Peptides
Glucocorticoid Receptors
Prefrontal Cortex
Dementia
Animal Models
Steroids
Phosphorylation
Learning
Hormones
Neurons
Brain

Keywords

  • Alzheimer Disease
  • Amyloid beta-Peptides
  • Animals
  • Brain
  • Cognitive Dysfunction
  • Glucocorticoids
  • Hippocampus
  • Humans
  • Hypothalamo-Hypophyseal System
  • Memory Disorders
  • Phosphorylation
  • Pituitary-Adrenal System
  • Protein Aggregation, Pathological
  • Receptors, Corticotropin-Releasing Hormone
  • tau Proteins
  • Journal Article
  • Review

Cite this

Endogenous glucocorticoids: role in the etiopathogenesis of Alzheimer's disease. / Libro, Rosaliana; Bramanti, Placido; Mazzon, Emanuela.

In: Neuroendocrinology Letters, Vol. 38, No. 1, 02.2017, p. 1-12.

Research output: Contribution to journalReview article

@article{6a0e9bc8bc2b43a4bbf8159374119453,
title = "Endogenous glucocorticoids: role in the etiopathogenesis of Alzheimer's disease",
abstract = "Endogenous glucocorticoids (eGCs) are steroid hormones with a wide spectrum of physiological effects. However, enhanced basal eGCs levels have been observed in patients affected by Alzheimer's disease (AD) and they have been correlated with dysregulation of the hypothalamic-pituitary-adrenocortical axis, hippocampal degeneration and reduced cognitive/memory performance. Therefore, it has been proposed that elevated concentration of eGCs might have a role in AD pathogenesis. AD is the most common form of dementia, characterized by the pathological accumulation of two proteins: the Amyloid Beta (Aβ) and the microtubule-associated protein tau in the neurons of the hippocampus and prefrontal cortex. In particular, the hippocampus, the cerebral area involved in learning and memory, is the brain region more vulnerable to chronic eGCs exposure. Although clinical studies have failed to establish a direct causative link between eGCs e and AD pathogenesis, evidences from pre-clinical studies have shown that increased eGCs levels accelerate the formation of Aβ in AD animal models by promoting the amyloidogenic pathway, and in parallel by reducing Aβ clearance, through transcriptional mechanisms involving the Glucocorticoid receptors. Instead, the effects of stress on tau phosphorylation seem to be mainly mediated bv the corticotropin-releasing factor receptor (CRFR1) and independent from stress-induced eGCs elevation.",
keywords = "Alzheimer Disease, Amyloid beta-Peptides, Animals, Brain, Cognitive Dysfunction, Glucocorticoids, Hippocampus, Humans, Hypothalamo-Hypophyseal System, Memory Disorders, Phosphorylation, Pituitary-Adrenal System, Protein Aggregation, Pathological, Receptors, Corticotropin-Releasing Hormone, tau Proteins, Journal Article, Review",
author = "Rosaliana Libro and Placido Bramanti and Emanuela Mazzon",
year = "2017",
month = "2",
language = "English",
volume = "38",
pages = "1--12",
journal = "Neuroendocrinology Letters",
issn = "0172-780X",
publisher = "Maghira and Maas Publications",
number = "1",

}

TY - JOUR

T1 - Endogenous glucocorticoids: role in the etiopathogenesis of Alzheimer's disease

AU - Libro, Rosaliana

AU - Bramanti, Placido

AU - Mazzon, Emanuela

PY - 2017/2

Y1 - 2017/2

N2 - Endogenous glucocorticoids (eGCs) are steroid hormones with a wide spectrum of physiological effects. However, enhanced basal eGCs levels have been observed in patients affected by Alzheimer's disease (AD) and they have been correlated with dysregulation of the hypothalamic-pituitary-adrenocortical axis, hippocampal degeneration and reduced cognitive/memory performance. Therefore, it has been proposed that elevated concentration of eGCs might have a role in AD pathogenesis. AD is the most common form of dementia, characterized by the pathological accumulation of two proteins: the Amyloid Beta (Aβ) and the microtubule-associated protein tau in the neurons of the hippocampus and prefrontal cortex. In particular, the hippocampus, the cerebral area involved in learning and memory, is the brain region more vulnerable to chronic eGCs exposure. Although clinical studies have failed to establish a direct causative link between eGCs e and AD pathogenesis, evidences from pre-clinical studies have shown that increased eGCs levels accelerate the formation of Aβ in AD animal models by promoting the amyloidogenic pathway, and in parallel by reducing Aβ clearance, through transcriptional mechanisms involving the Glucocorticoid receptors. Instead, the effects of stress on tau phosphorylation seem to be mainly mediated bv the corticotropin-releasing factor receptor (CRFR1) and independent from stress-induced eGCs elevation.

AB - Endogenous glucocorticoids (eGCs) are steroid hormones with a wide spectrum of physiological effects. However, enhanced basal eGCs levels have been observed in patients affected by Alzheimer's disease (AD) and they have been correlated with dysregulation of the hypothalamic-pituitary-adrenocortical axis, hippocampal degeneration and reduced cognitive/memory performance. Therefore, it has been proposed that elevated concentration of eGCs might have a role in AD pathogenesis. AD is the most common form of dementia, characterized by the pathological accumulation of two proteins: the Amyloid Beta (Aβ) and the microtubule-associated protein tau in the neurons of the hippocampus and prefrontal cortex. In particular, the hippocampus, the cerebral area involved in learning and memory, is the brain region more vulnerable to chronic eGCs exposure. Although clinical studies have failed to establish a direct causative link between eGCs e and AD pathogenesis, evidences from pre-clinical studies have shown that increased eGCs levels accelerate the formation of Aβ in AD animal models by promoting the amyloidogenic pathway, and in parallel by reducing Aβ clearance, through transcriptional mechanisms involving the Glucocorticoid receptors. Instead, the effects of stress on tau phosphorylation seem to be mainly mediated bv the corticotropin-releasing factor receptor (CRFR1) and independent from stress-induced eGCs elevation.

KW - Alzheimer Disease

KW - Amyloid beta-Peptides

KW - Animals

KW - Brain

KW - Cognitive Dysfunction

KW - Glucocorticoids

KW - Hippocampus

KW - Humans

KW - Hypothalamo-Hypophyseal System

KW - Memory Disorders

KW - Phosphorylation

KW - Pituitary-Adrenal System

KW - Protein Aggregation, Pathological

KW - Receptors, Corticotropin-Releasing Hormone

KW - tau Proteins

KW - Journal Article

KW - Review

M3 - Review article

C2 - 28456142

VL - 38

SP - 1

EP - 12

JO - Neuroendocrinology Letters

JF - Neuroendocrinology Letters

SN - 0172-780X

IS - 1

ER -