alexa Neuronal Plasticity in the Developing and Aging Cerebral Cortices of Patients with Down Syndrome
ISSN: 2376-0281

International Journal of Neurorehabilitation
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Research Article

Neuronal Plasticity in the Developing and Aging Cerebral Cortices of Patients with Down Syndrome

Miwa Takashima1,2*, Seiichiro Takahashi3, Osuke Iwata4, Sachiko Iwata4, Masahiro Yokoo1 and Sachio Takashima2,5

1Department of Physical Therapy, Yanagawa Rehabilitation School, Japan

2Graduate School, International University of Health and Welfare, Fukuoka, Japan

3Faculty of Rehabilitation, Kyushu Nutrition Welfare University, Fukuoka, Japan

4Department of Pediatrics, Kurume University school of Medicine, Fukuoka, Japan

5Yanagawa Institute for Developmental Disabilities, Fukuoka, Japan

*Corresponding Author:
Miwa Takashima
Department of Physical Therapy
Yanagawa Rehabilitation School
116-1, Kamimiyanag, Yanagawa
Fukuoka, 832-0058, Japan
Tel: +81944-72-1001
E-mail: [email protected]

Received date: June 02, 2014; Accepted date: July 25, 2014; Published date: August 15, 2014

Citation: Takashima M, Takahashi S, Iwata O, Iwata S, Yokoo M, et al. (2014) Neuronal Plasticity in the Developing and Aging Cerebral Cortices of Patients with Down Syndrome. Int J Neurorehabilitation 1:111. doi:10.4172/2376-0281.1000111

Copyright: © 2014 Takashima M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Background: The aim of the study was to clarify the developmental and aging changes of Protein gene product 9.5 (PGP9.5) expression in granular and pyramidal neurons of the cerebral cortex comparing patients with Down syndrome (DS) and subjects without it.

Subjects and Methods: Fifty-four human brains were obtained from post-mortem samples of 24 subjects with DS (19 weeks gestation (GW) to 63 years of age) and 30 subjects without it (20 GW to 75 years of age). PGP9.5 expression in the frontal cerebri was qualitatively assessed in specific cortical layers and compared among 4 age groups (fetus, infant, child, and adult), and between the brains with and without DS.

Results: In subjects without DS, the expression of PGP9.5 in the cerebral cortex was highest from 30 to 39 GW, and then decreased with increasing age. In patients with DS, cortical PGP9.5 expression did not decrease with aging. Compared with samples from subjects without DS, those from patients with DS showed weaker PGP9.5 expression in layers 3 and 5 (pyramidal cell layers) of the infant group, but stronger expression in layer 4 (granule cell layer) of the child group, and in layers 2, 3, 4, and 6 of the adult group.

Conclusion: An increase of PGP9.5 expression in cortical granule neurons from children to adults with DS was found and suggests the existence of an important therapeutic window during which compensatory and plastic processes may influence the progression of cognitive impairment in individuals with DS.

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