Neuroinflammation and neurodegeneration in overnutrition-induced diseases

Research output: Contribution to journalArticle

131 Citations (Scopus)

Abstract

Overnutrition-induced diseases such as obesity and type 2 diabetes (T2D) involve neural dysregulation of metabolic physiology. Recently, interdisciplinary research in neuroscience and immunology has linked overnutrition to a non-classical onset of inflammation in the brain, particularly in the hypothalamus. This neuroinflammation impairs central regulatory pathways of energy balance and nutrient metabolism, and leads to obesity, diabetes, and cardiovascular complications. This review describes recent findings on the roles of overnutrition-induced hypothalamic inflammation in neurodegeneration and defective adult neurogenesis, as well as in impaired neural stem cell regeneration, and their relevance to obesity and related diseases. In addition, commonalities in terms of neuroinflammation between neurodegenerative diseases and overnutrition-induced metabolic diseases are discussed. Targeting neuroinflammation and neurodegeneration will provide promising approaches for treating obesity and other overnutrition-related diseases.

Original languageEnglish (US)
Pages (from-to)40-47
Number of pages8
JournalTrends in Endocrinology and Metabolism
Volume24
Issue number1
DOIs
StatePublished - Jan 2013

Fingerprint

Overnutrition
Obesity
Neural Stem Cells
Metabolic Diseases
Neurogenesis
Encephalitis
Diabetes Complications
Neurosciences
Allergy and Immunology
Neurodegenerative Diseases
Type 2 Diabetes Mellitus
Hypothalamus
Regeneration
Inflammation
Food
Research

Keywords

  • Brain
  • Diabetes
  • Hypothalamus
  • Inflammation
  • Neural stem cells
  • Neurodegeneration
  • NF-κB
  • Obesity

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Neuroinflammation and neurodegeneration in overnutrition-induced diseases. / Cai, Dongsheng.

In: Trends in Endocrinology and Metabolism, Vol. 24, No. 1, 01.2013, p. 40-47.

Research output: Contribution to journalArticle

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