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Aging and sedentarism decrease vascularization and VEGF levels in the rat substantia nigra. Implications for

Begoña Villar-Cheda¹, Daniel Sousa-Ribeiro, Jannette Rodriguez-Pallares

¹Laboratory of Neuroanatomy and Experimental Neurology, Department of Morphological Sciences, Faculty of Medicine, University of Santiago de Compostela, Santiago de Compostela, Spain.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism

|October 30, 2008

Summary

This summary is machine-generated.

Aging decreases blood vessel density and vascular endothelial growth factor (VEGF) in the substantia nigra, increasing Parkinson's disease (PD) risk. Physical exercise reversed these changes, suggesting a protective effect against age-related neurodegeneration.

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Area of Science:

Neuroscience
Aging Research
Vascular Biology

Background:

Aging may alter nigral vascularization and vascular endothelial growth factor (VEGF) levels, potentially impacting Parkinson's disease (PD) risk.
Previous studies reported changes in PD, but the effects of aging alone are not well understood.

Purpose of the Study:

To investigate age-dependent changes in nigral microvessel density and VEGF mRNA expression in rats.
To determine if physical exercise can modulate these age-related changes.
To compare age-related changes with those observed in PD.

Main Methods:

Nonexercised and exercised rat models were used to study age-dependent changes.
Nigral microvessel density and VEGF mRNA expression were quantified.

Main Results:

Nonexercised rats showed age-dependent decreases in nigral microvessel density and VEGF mRNA expression.
Physical exercise reversed these age-related declines.
The observed age-related pattern was opposite to that seen in PD.

Conclusions:

Age-related decline in nigral vascularization and VEGF may increase vulnerability to dopaminergic neurodegeneration and PD risk.
Physical exercise may mitigate these age-related risks.
The underlying process of PD may not be solely an accelerated form of age-dependent decline.