Affiliations: [a] Section for Psychiatry and Neurochemistry, Neuropsychiatric Epidemiology Unit at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden | [b] Departments of Neurology and Medicine, State University of New York-Downstate Medical Center, Brooklyn, NY, USA
Correspondence:
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Correspondence to: Deborah Gustafson, MS, PhD, Institute for Neuroscience and Physiology, Section for Psychiatry and Neurochemistry, Wallinsgatan 6, Mölndal 431 41, Sweden. Tel.: +46 31 343 8646; Fax: +46 31 776 04 03; E-mail: deborah.gustafson@neuro.gu.se; Departments of Neurology and Medicine, Section for NeuroEpidemiology, 450 Clarkson Avenue, Brooklyn, NY 11203, USA. Tel.: +1 718 270 1581; Fax: +1 718 270 3840; E-mail: deborah.gustafson@downstate.edu.
Abstract: Level of adiposity is linked to manifest dementia and Alzheimer's disease in epidemiological studies. Overweight and obesity in mid- and late-life may increase risk for dementia, whereas decline in body weight or body mass index and underweight in years preceding and at the time of a dementia diagnosis may also relate to dementia. The role of adiposity during the period of cognitive decline is, as yet, not understood; however, some hypotheses relating adipose tissue to brain can be drawn. This review focuses on potential, varied mechanisms whereby adipose tissue may influence or interact with the brain and/or dementia risk during the dynamic period of life characterized by both body weight and cognitive decline. These mechanisms relate to: a) adipose tissue location and cell types, b) body composition, c) endocrine adipose, and d) the interplay among adipose, brain structure and function, and genes. This review will illustrate that adipose tissue is a quintessential, multifunctional tissue of the human body.
