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Updated: Jun 8, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Adiposity hormones and dementia.

Deborah R Gustafson¹

¹Section for Psychiatry and Neurochemistry, Neuropsychiatric Epidemiology Unit at the Sahlgrenska Academy, University of Gothenburg, Sweden. deborah.gustafson@neuro.gu.se

Journal of the Neurological Sciences

|September 30, 2010

Summary

This summary is machine-generated.

Excess adipose tissue contributes to vascular risk and dementia. Hormones from fat, like leptin and adiponectin, interact with the brain, influencing dementia development and progression.

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Area of Science:

Endocrinology
Neuroscience
Metabolic Syndrome

Background:

Adipose tissue functions as an endocrine organ impacting metabolic and vascular health.
Obesity is a significant risk factor for vascular disease and late-onset dementia.
Vascular risk is linked to hormonal and metabolic dysregulation, potentially preceding or resulting from dementia.

Purpose of the Study:

To review the epidemiology of adiposity and dementia.
To explore adipose tissue biology and its key hormones, leptin and adiponectin.
To synthesize evidence on the role of adipose hormones in dementia.

Main Methods:

Literature review of epidemiological data on adiposity and dementia.
Analysis of adipose tissue endocrine functions.
Examination of leptin and adiponectin interactions with the brain.

Main Results:

Adiposity is a cornerstone of vascular risk, increasing dementia incidence.
Hormonal alterations associated with obesity may precede or arise from dementia.
Leptin and adiponectin, produced by adipose tissue, directly influence brain function.

Conclusions:

Adipose tissue plays a critical role in brain health and dementia processes.
Understanding adipose hormones is crucial for comprehending dementia.
Metabolic and hormonal factors are integral to dementia pathogenesis.