Integrative neurobiology of metabolic diseases, neuroinflammation, and neurodegeneration

Gertjan van Dijk, S. van Heijningen, A. C. Reijne, C. Nyakas, E. A. van der Zee, U. L M Eisel

Research output: Contribution to journalArticle

41 Citations (Scopus)

Abstract

Alzheimer's disease (AD) is a complex, multifactorial disease with a number of leading mechanisms, including neuroinflammation, processing of amyloid precursor protein (APP) to amyloid β peptide, tau protein hyperphosphorylation, relocalization and deposition. These mechanisms are propagated by obesity, the metabolic syndrome and type-2 diabetes mellitus. Stress, sedentariness, dietary overconsumption of saturated fat and refined sugars, and circadian derangements/disturbed sleep contribute to obesity and related metabolic diseases, but also accelerate age-related damage and senescence that all feed the risk of developing AD too. The complex and interacting mechanisms are not yet completely understood and will require further analysis. Instead of investigating AD as a mono- or oligocausal disease we should address the disease by understanding the multiple underlying mechanisms and how these interact. Future research therefore might concentrate on integrating these by "systems biology" approaches, but also to regard them from an evolutionary medicine point of view. The current review addresses several of these interacting mechanisms in animal models and compares them with clinical data giving an overview about our current knowledge and puts them into an integrated framework.

Original languageEnglish
Article number173
JournalFrontiers in Neuroscience
Volume9
Issue numberAPR
DOIs
Publication statusPublished - Apr 28 2015

Fingerprint

Neurobiology
Metabolic Diseases
Alzheimer Disease
Obesity
tau Proteins
Systems Biology
Amyloid beta-Protein Precursor
Amyloid
Type 2 Diabetes Mellitus
Sleep
Animal Models
Fats
Medicine
Peptides

Keywords

  • Aging
  • Alzheimer's disease
  • Blood-brain barrier
  • Metabolic syndrome
  • Neuroinflammation
  • Obesity
  • Tnf
  • Type-2 diabetes mellitus

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

van Dijk, G., van Heijningen, S., Reijne, A. C., Nyakas, C., van der Zee, E. A., & Eisel, U. L. M. (2015). Integrative neurobiology of metabolic diseases, neuroinflammation, and neurodegeneration. Frontiers in Neuroscience, 9(APR), [173]. https://doi.org/10.3389/fnins.2015.00173

Integrative neurobiology of metabolic diseases, neuroinflammation, and neurodegeneration. / van Dijk, Gertjan; van Heijningen, S.; Reijne, A. C.; Nyakas, C.; van der Zee, E. A.; Eisel, U. L M.

In: Frontiers in Neuroscience, Vol. 9, No. APR, 173, 28.04.2015.

Research output: Contribution to journalArticle

van Dijk, Gertjan ; van Heijningen, S. ; Reijne, A. C. ; Nyakas, C. ; van der Zee, E. A. ; Eisel, U. L M. / Integrative neurobiology of metabolic diseases, neuroinflammation, and neurodegeneration. In: Frontiers in Neuroscience. 2015 ; Vol. 9, No. APR.
@article{8f00748ec0084422a92cc84446cc8831,
title = "Integrative neurobiology of metabolic diseases, neuroinflammation, and neurodegeneration",
abstract = "Alzheimer's disease (AD) is a complex, multifactorial disease with a number of leading mechanisms, including neuroinflammation, processing of amyloid precursor protein (APP) to amyloid β peptide, tau protein hyperphosphorylation, relocalization and deposition. These mechanisms are propagated by obesity, the metabolic syndrome and type-2 diabetes mellitus. Stress, sedentariness, dietary overconsumption of saturated fat and refined sugars, and circadian derangements/disturbed sleep contribute to obesity and related metabolic diseases, but also accelerate age-related damage and senescence that all feed the risk of developing AD too. The complex and interacting mechanisms are not yet completely understood and will require further analysis. Instead of investigating AD as a mono- or oligocausal disease we should address the disease by understanding the multiple underlying mechanisms and how these interact. Future research therefore might concentrate on integrating these by {"}systems biology{"} approaches, but also to regard them from an evolutionary medicine point of view. The current review addresses several of these interacting mechanisms in animal models and compares them with clinical data giving an overview about our current knowledge and puts them into an integrated framework.",
keywords = "Aging, Alzheimer's disease, Blood-brain barrier, Metabolic syndrome, Neuroinflammation, Obesity, Tnf, Type-2 diabetes mellitus",
author = "{van Dijk}, Gertjan and {van Heijningen}, S. and Reijne, {A. C.} and C. Nyakas and {van der Zee}, {E. A.} and Eisel, {U. L M}",
year = "2015",
month = "4",
day = "28",
doi = "10.3389/fnins.2015.00173",
language = "English",
volume = "9",
journal = "Frontiers in Neuroscience",
issn = "1662-4548",
publisher = "Frontiers Research Foundation",
number = "APR",

}

TY - JOUR

T1 - Integrative neurobiology of metabolic diseases, neuroinflammation, and neurodegeneration

AU - van Dijk, Gertjan

AU - van Heijningen, S.

AU - Reijne, A. C.

AU - Nyakas, C.

AU - van der Zee, E. A.

AU - Eisel, U. L M

PY - 2015/4/28

Y1 - 2015/4/28

N2 - Alzheimer's disease (AD) is a complex, multifactorial disease with a number of leading mechanisms, including neuroinflammation, processing of amyloid precursor protein (APP) to amyloid β peptide, tau protein hyperphosphorylation, relocalization and deposition. These mechanisms are propagated by obesity, the metabolic syndrome and type-2 diabetes mellitus. Stress, sedentariness, dietary overconsumption of saturated fat and refined sugars, and circadian derangements/disturbed sleep contribute to obesity and related metabolic diseases, but also accelerate age-related damage and senescence that all feed the risk of developing AD too. The complex and interacting mechanisms are not yet completely understood and will require further analysis. Instead of investigating AD as a mono- or oligocausal disease we should address the disease by understanding the multiple underlying mechanisms and how these interact. Future research therefore might concentrate on integrating these by "systems biology" approaches, but also to regard them from an evolutionary medicine point of view. The current review addresses several of these interacting mechanisms in animal models and compares them with clinical data giving an overview about our current knowledge and puts them into an integrated framework.

AB - Alzheimer's disease (AD) is a complex, multifactorial disease with a number of leading mechanisms, including neuroinflammation, processing of amyloid precursor protein (APP) to amyloid β peptide, tau protein hyperphosphorylation, relocalization and deposition. These mechanisms are propagated by obesity, the metabolic syndrome and type-2 diabetes mellitus. Stress, sedentariness, dietary overconsumption of saturated fat and refined sugars, and circadian derangements/disturbed sleep contribute to obesity and related metabolic diseases, but also accelerate age-related damage and senescence that all feed the risk of developing AD too. The complex and interacting mechanisms are not yet completely understood and will require further analysis. Instead of investigating AD as a mono- or oligocausal disease we should address the disease by understanding the multiple underlying mechanisms and how these interact. Future research therefore might concentrate on integrating these by "systems biology" approaches, but also to regard them from an evolutionary medicine point of view. The current review addresses several of these interacting mechanisms in animal models and compares them with clinical data giving an overview about our current knowledge and puts them into an integrated framework.

KW - Aging

KW - Alzheimer's disease

KW - Blood-brain barrier

KW - Metabolic syndrome

KW - Neuroinflammation

KW - Obesity

KW - Tnf

KW - Type-2 diabetes mellitus

UR - http://www.scopus.com/inward/record.url?scp=84928746179&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84928746179&partnerID=8YFLogxK

U2 - 10.3389/fnins.2015.00173

DO - 10.3389/fnins.2015.00173

M3 - Article

AN - SCOPUS:84928746179

VL - 9

JO - Frontiers in Neuroscience

JF - Frontiers in Neuroscience

SN - 1662-4548

IS - APR

M1 - 173

ER -