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Cell Tissue Res. 2018 Jan;371(1):105-113. doi: 10.1007/s00441-017-2715-8. Epub 2017 Nov 9.

The systemic environment: at the interface of aging and adult neurogenesis.

Smith LK1,2,3, White CW 3rd1,2,4, Villeda SA5,6,7,8.

Author information

1
Department of Anatomy, University of California, San Francisco, San Francisco, CA, 94143, USA.
2
The Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California San Francisco, San Francisco, CA, 94143, USA.
3
Biomedical Sciences Graduate Program, University of California San Francisco, San Francisco, CA, 94143, USA.
4
Developmental and Stem Cell Biology Graduate Program, University of California San Francisco, San Francisco, CA, 94143, USA.
5
Department of Anatomy, University of California, San Francisco, San Francisco, CA, 94143, USA. saul.villeda@ucsf.edu.
6
The Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California San Francisco, San Francisco, CA, 94143, USA. saul.villeda@ucsf.edu.
7
Biomedical Sciences Graduate Program, University of California San Francisco, San Francisco, CA, 94143, USA. saul.villeda@ucsf.edu.
8
Developmental and Stem Cell Biology Graduate Program, University of California San Francisco, San Francisco, CA, 94143, USA. saul.villeda@ucsf.edu.

Abstract

Aging results in impaired neurogenesis in the two neurogenic niches of the adult mammalian brain, the dentate gyrus of the hippocampus and the subventricular zone of the lateral ventricle. While significant work has characterized intrinsic cellular changes that contribute to this decline, it is increasingly apparent that the systemic environment also represents a critical driver of brain aging. Indeed, emerging studies utilizing the model of heterochronic parabiosis have revealed that immune-related molecular and cellular changes in the aging systemic environment negatively regulate adult neurogenesis. Interestingly, these studies have also demonstrated that age-related decline in neurogenesis can be ameliorated by exposure to the young systemic environment. While this burgeoning field of research is increasingly garnering interest, as yet, the precise mechanisms driving either the pro-aging effects of aged blood or the rejuvenating effects of young blood remain to be thoroughly defined. Here, we review how age-related changes in blood, blood-borne factors, and peripheral immune cells contribute to the age-related decline in adult neurogenesis in the mammalian brain, and posit both direct neural stem cell and indirect neurogenic niche-mediated mechanisms.

KEYWORDS:

Adult neurogenesis; Aging; Blood; Immune cells; Rejuvenation

PMID:
29124393
PMCID:
PMC5748432
DOI:
10.1007/s00441-017-2715-8
[Indexed for MEDLINE]
Free PMC Article

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