Pathophysiological Links Among Hypertension and Alzheimer’s Disease

Daniela Carnevale, Marialuisa Perrotta, Giuseppe Lembo, Bruno Trimarco

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Genetic Alzheimer’s disease (AD) accounts for only few AD cases and is almost exclusively associated to increased amyloid production in the brain. Instead, the majority of patients is affected with the AD sporadic form with typical alterations of clearance mechanisms of the brain. Most studies use engineered animal models that mimic genetic AD. Since it is emerging the existence of a pathophysiological link between cardiovascular risk factors and AD etiology, the strategy to develop animal models of vascular related AD pathology could be the key toward developing novel successful therapies. On this issue, we have demonstrated that mice that have been chronically subjected to high blood pressure show deposition of amyloid aggregates, the main histological feature of AD, and loss of memory in specific tasks. More importantly, we have identified that the hypertensive challenge increases the expression of the receptor for advanced glycated end products (RAGE), leading to beta-amyloid (Aβ) deposition and learning impairment. Here, we review different murine models of hypertension, induced either pharmacologically or mechanically, leading in the long time to plaque formation in the brain parenchyma and around blood vessels. The major findings obtained till now in this particular experimental setting allow us to suggest that this appears to be a unique possibility to study the pathogenetic mechanisms of sporadic AD triggered by vascular risk factors.

Original languageEnglish
Pages (from-to)3-7
Number of pages5
JournalHigh Blood Pressure and Cardiovascular Prevention
Volume23
Issue number1
DOIs
Publication statusPublished - Mar 1 2016

Fingerprint

Alzheimer Disease
Hypertension
Amyloid
Inborn Genetic Diseases
Blood Vessels
Brain
Animal Models
Memory Disorders
Learning
Pathology

Keywords

  • Alzheimer’s disease (AD)
  • Beta-amyloid (Aβ) deposition and cognitive impairment
  • Hypertension and cardiovascular risk factors
  • Murine models of vascular-related AD
  • RAGE, receptor for advanced glycated end products

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Internal Medicine

Cite this

Pathophysiological Links Among Hypertension and Alzheimer’s Disease. / Carnevale, Daniela; Perrotta, Marialuisa; Lembo, Giuseppe; Trimarco, Bruno.

In: High Blood Pressure and Cardiovascular Prevention, Vol. 23, No. 1, 01.03.2016, p. 3-7.

Research output: Contribution to journalArticle

@article{730f1f4ab1774c5fb2feb0f48acc3c4f,
title = "Pathophysiological Links Among Hypertension and Alzheimer’s Disease",
abstract = "Genetic Alzheimer’s disease (AD) accounts for only few AD cases and is almost exclusively associated to increased amyloid production in the brain. Instead, the majority of patients is affected with the AD sporadic form with typical alterations of clearance mechanisms of the brain. Most studies use engineered animal models that mimic genetic AD. Since it is emerging the existence of a pathophysiological link between cardiovascular risk factors and AD etiology, the strategy to develop animal models of vascular related AD pathology could be the key toward developing novel successful therapies. On this issue, we have demonstrated that mice that have been chronically subjected to high blood pressure show deposition of amyloid aggregates, the main histological feature of AD, and loss of memory in specific tasks. More importantly, we have identified that the hypertensive challenge increases the expression of the receptor for advanced glycated end products (RAGE), leading to beta-amyloid (Aβ) deposition and learning impairment. Here, we review different murine models of hypertension, induced either pharmacologically or mechanically, leading in the long time to plaque formation in the brain parenchyma and around blood vessels. The major findings obtained till now in this particular experimental setting allow us to suggest that this appears to be a unique possibility to study the pathogenetic mechanisms of sporadic AD triggered by vascular risk factors.",
keywords = "Alzheimer’s disease (AD), Beta-amyloid (Aβ) deposition and cognitive impairment, Hypertension and cardiovascular risk factors, Murine models of vascular-related AD, RAGE, receptor for advanced glycated end products",
author = "Daniela Carnevale and Marialuisa Perrotta and Giuseppe Lembo and Bruno Trimarco",
year = "2016",
month = "3",
day = "1",
doi = "10.1007/s40292-015-0108-1",
language = "English",
volume = "23",
pages = "3--7",
journal = "High Blood Pressure and Cardiovascular Prevention",
issn = "1120-9879",
publisher = "Adis International Ltd",
number = "1",

}

TY - JOUR

T1 - Pathophysiological Links Among Hypertension and Alzheimer’s Disease

AU - Carnevale, Daniela

AU - Perrotta, Marialuisa

AU - Lembo, Giuseppe

AU - Trimarco, Bruno

PY - 2016/3/1

Y1 - 2016/3/1

N2 - Genetic Alzheimer’s disease (AD) accounts for only few AD cases and is almost exclusively associated to increased amyloid production in the brain. Instead, the majority of patients is affected with the AD sporadic form with typical alterations of clearance mechanisms of the brain. Most studies use engineered animal models that mimic genetic AD. Since it is emerging the existence of a pathophysiological link between cardiovascular risk factors and AD etiology, the strategy to develop animal models of vascular related AD pathology could be the key toward developing novel successful therapies. On this issue, we have demonstrated that mice that have been chronically subjected to high blood pressure show deposition of amyloid aggregates, the main histological feature of AD, and loss of memory in specific tasks. More importantly, we have identified that the hypertensive challenge increases the expression of the receptor for advanced glycated end products (RAGE), leading to beta-amyloid (Aβ) deposition and learning impairment. Here, we review different murine models of hypertension, induced either pharmacologically or mechanically, leading in the long time to plaque formation in the brain parenchyma and around blood vessels. The major findings obtained till now in this particular experimental setting allow us to suggest that this appears to be a unique possibility to study the pathogenetic mechanisms of sporadic AD triggered by vascular risk factors.

AB - Genetic Alzheimer’s disease (AD) accounts for only few AD cases and is almost exclusively associated to increased amyloid production in the brain. Instead, the majority of patients is affected with the AD sporadic form with typical alterations of clearance mechanisms of the brain. Most studies use engineered animal models that mimic genetic AD. Since it is emerging the existence of a pathophysiological link between cardiovascular risk factors and AD etiology, the strategy to develop animal models of vascular related AD pathology could be the key toward developing novel successful therapies. On this issue, we have demonstrated that mice that have been chronically subjected to high blood pressure show deposition of amyloid aggregates, the main histological feature of AD, and loss of memory in specific tasks. More importantly, we have identified that the hypertensive challenge increases the expression of the receptor for advanced glycated end products (RAGE), leading to beta-amyloid (Aβ) deposition and learning impairment. Here, we review different murine models of hypertension, induced either pharmacologically or mechanically, leading in the long time to plaque formation in the brain parenchyma and around blood vessels. The major findings obtained till now in this particular experimental setting allow us to suggest that this appears to be a unique possibility to study the pathogenetic mechanisms of sporadic AD triggered by vascular risk factors.

KW - Alzheimer’s disease (AD)

KW - Beta-amyloid (Aβ) deposition and cognitive impairment

KW - Hypertension and cardiovascular risk factors

KW - Murine models of vascular-related AD

KW - RAGE, receptor for advanced glycated end products

UR - http://www.scopus.com/inward/record.url?scp=84961259127&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84961259127&partnerID=8YFLogxK

U2 - 10.1007/s40292-015-0108-1

DO - 10.1007/s40292-015-0108-1

M3 - Article

AN - SCOPUS:84961259127

VL - 23

SP - 3

EP - 7

JO - High Blood Pressure and Cardiovascular Prevention

JF - High Blood Pressure and Cardiovascular Prevention

SN - 1120-9879

IS - 1

ER -