Chronic Hypertension Leads to Neurodegeneration in the TgSwDI Mouse Model of Alzheimer’s Disease

Numerous epidemiological studies link vascular disorders, such as hypertension, diabetes mellitus, and stroke, with Alzheimer’s disease (AD). Hypertension, specifically, is an important modifiable risk factor for late-onset AD. To examine the link between midlife hypertension and the onset of AD lat...

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Published inHypertension (Dallas, Tex. 1979) Vol. 66; no. 1; pp. 175 - 182
Main Authors Kruyer, Anna, Soplop, Nadine, Strickland, Sidney, Norris, Erin H
Format Journal Article
LanguageEnglish
Published United States American Heart Association, Inc 01.07.2015
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Abstract Numerous epidemiological studies link vascular disorders, such as hypertension, diabetes mellitus, and stroke, with Alzheimer’s disease (AD). Hypertension, specifically, is an important modifiable risk factor for late-onset AD. To examine the link between midlife hypertension and the onset of AD later in life, we chemically induced chronic hypertension in the TgSwDI mouse model of AD in early adulthood. Hypertension accelerated cognitive deficits in the Barnes maze test (P<0.05 after 3 months of treatment; P<0.001 after 6 months), microvascular deposition of β-amyloid (P<0.001 after 3 months of treatment; P<0.05 after 6 months), vascular inflammation (P<0.05 in the dentate gyrus and P<0.001 in the dorsal subiculum after 6 months of treatment), blood–brain barrier leakage (P<0.05 after 3 and 6 months of treatment), and pericyte loss (P<0.05 in the dentate gyrus and P<0.01 in the dorsal subiculum after 6 months of treatment) in these mice. In addition, hypertension induced hippocampal neurodegeneration at an early age in this mouse line (43% reduction in the dorsal subiculum; P<0.05), establishing this as a useful research model of AD with mixed vascular and amyloid pathologies.
AbstractList Numerous epidemiological studies link vascular disorders, such as hypertension, diabetes mellitus, and stroke, with Alzheimer’s disease (AD). Hypertension, specifically, is an important modifiable risk factor for late-onset AD. To examine the link between midlife hypertension and the onset of AD later in life, we chemically induced chronic hypertension in the TgSwDI mouse model of AD in early adulthood. Hypertension accelerated cognitive deficits in the Barnes maze test (P<0.05 after 3 months of treatment; P<0.001 after 6 months), microvascular deposition of β-amyloid (P<0.001 after 3 months of treatment; P<0.05 after 6 months), vascular inflammation (P<0.05 in the dentate gyrus and P<0.001 in the dorsal subiculum after 6 months of treatment), blood–brain barrier leakage (P<0.05 after 3 and 6 months of treatment), and pericyte loss (P<0.05 in the dentate gyrus and P<0.01 in the dorsal subiculum after 6 months of treatment) in these mice. In addition, hypertension induced hippocampal neurodegeneration at an early age in this mouse line (43% reduction in the dorsal subiculum; P<0.05), establishing this as a useful research model of AD with mixed vascular and amyloid pathologies.
Numerous epidemiological studies link vascular disorders, such as hypertension, diabetes mellitus, and stroke, with Alzheimer’s disease (AD). Hypertension, specifically, is an important modifiable risk factor for late-onset AD. To examine the link between midlife hypertension and the onset of AD later in life, we chemically induced chronic hypertension in the TgSwDI mouse model of AD in early adulthood. Hypertension accelerated cognitive deficits in the Barnes maze test ( P <0.05 after 3 months of treatment; P <0.001 after 6 months), microvascular deposition of β-amyloid ( P <0.001 after 3 months of treatment; P <0.05 after 6 months), vascular inflammation ( P <0.05 in the dentate gyrus and P <0.001 in the dorsal subiculum after 6 months of treatment), blood–brain barrier leakage ( P <0.05 after 3 and 6 months of treatment), and pericyte loss ( P <0.05 in the dentate gyrus and P <0.01 in the dorsal subiculum after 6 months of treatment) in these mice. In addition, hypertension induced hippocampal neurodegeneration at an early age in this mouse line (43% reduction in the dorsal subiculum; P <0.05), establishing this as a useful research model of AD with mixed vascular and amyloid pathologies.
Numerous epidemiological studies link vascular disorders, such as hypertension, diabetes mellitus, and stroke, with Alzheimer's disease (AD). Hypertension, specifically, is an important modifiable risk factor for late-onset AD. To examine the link between midlife hypertension and the onset of AD later in life, we chemically induced chronic hypertension in the TgSwDI mouse model of AD in early adulthood. Hypertension accelerated cognitive deficits in the Barnes maze test (P&lt;0.05 after 3 months of treatment; P&lt;0.001 after 6 months), microvascular deposition of β-amyloid (P&lt;0.001 after 3 months of treatment; P&lt;0.05 after 6 months), vascular inflammation (P&lt;0.05 in the dentate gyrus and P&lt;0.001 in the dorsal subiculum after 6 months of treatment), blood-brain barrier leakage (P&lt;0.05 after 3 and 6 months of treatment), and pericyte loss (P&lt;0.05 in the dentate gyrus and P&lt;0.01 in the dorsal subiculum after 6 months of treatment) in these mice. In addition, hypertension induced hippocampal neurodegeneration at an early age in this mouse line (43% reduction in the dorsal subiculum; P&lt;0.05), establishing this as a useful research model of AD with mixed vascular and amyloid pathologies.
Numerous epidemiological studies link vascular disorders, such as hypertension, diabetes, and stroke, with Alzheimer’s disease. Hypertension, specifically, is an important modifiable risk factor for late onset Alzheimer’s disease. To examine the link between midlife hypertension and the onset of Alzheimer’s disease later in life, we chemically induced chronic hypertension in the TgSwDI mouse model of Alzheimer’s disease in early adulthood. Hypertension accelerated cognitive deficits in the Barnes maze test (p<0.05 after 3 months of treatment; p<0.001 after 6 months), microvascular deposition of beta-amyloid (p<0.001 after 3 months of treatment; p<0.05 after 6 months), vascular inflammation (p<0.05 in the dentate gyrus and p<0.001 in the dorsal subiculum after 6 months of treatment), blood brain barrier leakage (p<0.05 after 3 and 6 months of treatment), and pericyte loss (p<0.05 in the dentate gyrus and p<0.01 in the dorsal subiculum after 6 months of treatment) in these mice. Additionally, hypertension induced hippocampal neurodegeneration at an early age in this mouse line (43% reduction in the dorsal subiculum, p<0.05), establishing this as a useful research model of Alzheimer’s disease with mixed vascular and amyloid pathologies.
Author Soplop, Nadine
Strickland, Sidney
Kruyer, Anna
Norris, Erin H
AuthorAffiliation From the Patricia and John Rosenwald Laboratory of Neurobiology and Genetics (A.K., S.S., E.H.N.), Electron Microscopy Resource Center (N.S.), The Rockefeller University, New York, NY
AuthorAffiliation_xml – name: From the Patricia and John Rosenwald Laboratory of Neurobiology and Genetics (A.K., S.S., E.H.N.), Electron Microscopy Resource Center (N.S.), The Rockefeller University, New York, NY
– name: 2 The Rockefeller University, Electron Microscopy Resource Center
– name: 1 The Rockefeller University, Patricia and John Rosenwald Laboratory of Neurobiology and Genetics
Author_xml – sequence: 1
  givenname: Anna
  surname: Kruyer
  fullname: Kruyer, Anna
  organization: From the Patricia and John Rosenwald Laboratory of Neurobiology and Genetics (A.K., S.S., E.H.N.), Electron Microscopy Resource Center (N.S.), The Rockefeller University, New York, NY
– sequence: 2
  givenname: Nadine
  surname: Soplop
  fullname: Soplop, Nadine
– sequence: 3
  givenname: Sidney
  surname: Strickland
  fullname: Strickland, Sidney
– sequence: 4
  givenname: Erin
  surname: Norris
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  fullname: Norris, Erin H
BackLink https://www.ncbi.nlm.nih.gov/pubmed/25941345$$D View this record in MEDLINE/PubMed
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Keywords cerebral amyloid angiopathy
hypertension
blood–brain barrier
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Snippet Numerous epidemiological studies link vascular disorders, such as hypertension, diabetes mellitus, and stroke, with Alzheimer’s disease (AD). Hypertension,...
Numerous epidemiological studies link vascular disorders, such as hypertension, diabetes mellitus, and stroke, with Alzheimer's disease (AD). Hypertension,...
Numerous epidemiological studies link vascular disorders, such as hypertension, diabetes, and stroke, with Alzheimer’s disease. Hypertension, specifically, is...
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StartPage 175
SubjectTerms Age of Onset
Alzheimer Disease - genetics
Amyloid beta-Peptides - analysis
Amyloid beta-Protein Precursor - genetics
Animals
Blood-Brain Barrier
Brain - blood supply
Cerebral Amyloid Angiopathy - etiology
Cerebral Amyloid Angiopathy - pathology
Chronic Disease
Dementia, Vascular - etiology
Dementia, Vascular - physiopathology
Disease Models, Animal
Female
Hippocampus - pathology
Humans
Hypertension - chemically induced
Hypertension - complications
Hypertension - physiopathology
Male
Maze Learning
Mice
Mice, Inbred C57BL
Mice, Transgenic
Microvessels - chemistry
Microvessels - pathology
Mutation
Nerve Degeneration - etiology
Nerve Degeneration - physiopathology
NG-Nitroarginine Methyl Ester - toxicity
Pericytes - pathology
Vasculitis - etiology
Vasculitis - physiopathology
Title Chronic Hypertension Leads to Neurodegeneration in the TgSwDI Mouse Model of Alzheimer’s Disease
URI https://www.ncbi.nlm.nih.gov/pubmed/25941345
https://search.proquest.com/docview/1687997226
https://pubmed.ncbi.nlm.nih.gov/PMC4465852
Volume 66
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