Long-Term Exercise Improves Memory Deficits via Restoration of Myelin and Microvessel Damage, and Enhancement of Neurogenesis in the Aged Gerbil Hippocampus after Ischemic Stroke

Ji Hyeon Ahn, Jung Hoon Choi, Joon Ha Park, In Hye Kim, Jeong Hwi Cho, Jae Chul Lee, Hyun Mo Koo, Gak Hwangbo, Ki Yeon Yoo, Choong Hyun Lee, In Koo Hwang, Jun Hwi Cho, Soo Young Choi, Young Guen Kwon, Young Myeong Kim, Il Jun Kang, Moo Ho Won

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Background. The positive correlation between therapeutic exercise and memory recovery in cases of ischemia has been extensively studied; however, long-term exercise begun after ischemic neuronal death as a chronic neurorestorative strategy has not yet been thoroughly examined. Objective. The purpose of this study is to investigate possible mechanisms by which exercise ameliorates ischemia-induced memory impairment in the aged gerbil hippocampus after transient cerebral ischemia. Methods. Treadmill exercise was begun 5 days after ischemia-reperfusion (I-R) and lasted for 1 or 4 weeks. The animals were sacrificed 31 days after the induction of ischemia. Changes in short-term memory, as well as the hippocampal expression of markers of cell proliferation, neuroblast differentiation, neurogenesis, myelin and microvessel repair, and growth factors were examined by immunohistochemistry and/or western blots. Results. Four weeks of exercise facilitated memory recovery despite neuronal damage in the stratum pyramidale (SP) of the hippocampal CA1 region and in the polymorphic layer (PoL) of the dentate gyrus (DG) after I-R. Long-term exercise enhanced cell proliferation and neuroblast differentiation in a time-dependent manner, and newly generated mature cells were found in the granule cell layer of the DG, but not in the SP of the CA1 region or in the PoL of the DG. In addition, long-term exercise ameliorated ischemia-induced damage of myelin and microvessels, which was correlated with increased BDNF expression in the CA1 region and the DG. Conclusions. These results suggest that long-term treadmill exercise after I-R can restore memory function through replacement of multiple damaged structures in the ischemic aged hippocampus.

Original languageEnglish
Pages (from-to)894-905
Number of pages12
JournalNeurorehabilitation and Neural Repair
Volume30
Issue number9
DOIs
Publication statusPublished - 2016 Oct 1

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Gerbillinae
Neurogenesis
Memory Disorders
Myelin Sheath
Microvessels
Hippocampus
Ischemia
Stroke
Dentate Gyrus
Hippocampal CA1 Region
Reperfusion
Cell Proliferation
Brain-Derived Neurotrophic Factor
Transient Ischemic Attack
Short-Term Memory
Intercellular Signaling Peptides and Proteins
Western Blotting
Immunohistochemistry

All Science Journal Classification (ASJC) codes

  • Rehabilitation
  • Neurology
  • Clinical Neurology

Cite this

Ahn, Ji Hyeon ; Choi, Jung Hoon ; Park, Joon Ha ; Kim, In Hye ; Cho, Jeong Hwi ; Lee, Jae Chul ; Koo, Hyun Mo ; Hwangbo, Gak ; Yoo, Ki Yeon ; Lee, Choong Hyun ; Hwang, In Koo ; Cho, Jun Hwi ; Choi, Soo Young ; Kwon, Young Guen ; Kim, Young Myeong ; Kang, Il Jun ; Won, Moo Ho. / Long-Term Exercise Improves Memory Deficits via Restoration of Myelin and Microvessel Damage, and Enhancement of Neurogenesis in the Aged Gerbil Hippocampus after Ischemic Stroke. In: Neurorehabilitation and Neural Repair. 2016 ; Vol. 30, No. 9. pp. 894-905.
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title = "Long-Term Exercise Improves Memory Deficits via Restoration of Myelin and Microvessel Damage, and Enhancement of Neurogenesis in the Aged Gerbil Hippocampus after Ischemic Stroke",
abstract = "Background. The positive correlation between therapeutic exercise and memory recovery in cases of ischemia has been extensively studied; however, long-term exercise begun after ischemic neuronal death as a chronic neurorestorative strategy has not yet been thoroughly examined. Objective. The purpose of this study is to investigate possible mechanisms by which exercise ameliorates ischemia-induced memory impairment in the aged gerbil hippocampus after transient cerebral ischemia. Methods. Treadmill exercise was begun 5 days after ischemia-reperfusion (I-R) and lasted for 1 or 4 weeks. The animals were sacrificed 31 days after the induction of ischemia. Changes in short-term memory, as well as the hippocampal expression of markers of cell proliferation, neuroblast differentiation, neurogenesis, myelin and microvessel repair, and growth factors were examined by immunohistochemistry and/or western blots. Results. Four weeks of exercise facilitated memory recovery despite neuronal damage in the stratum pyramidale (SP) of the hippocampal CA1 region and in the polymorphic layer (PoL) of the dentate gyrus (DG) after I-R. Long-term exercise enhanced cell proliferation and neuroblast differentiation in a time-dependent manner, and newly generated mature cells were found in the granule cell layer of the DG, but not in the SP of the CA1 region or in the PoL of the DG. In addition, long-term exercise ameliorated ischemia-induced damage of myelin and microvessels, which was correlated with increased BDNF expression in the CA1 region and the DG. Conclusions. These results suggest that long-term treadmill exercise after I-R can restore memory function through replacement of multiple damaged structures in the ischemic aged hippocampus.",
author = "Ahn, {Ji Hyeon} and Choi, {Jung Hoon} and Park, {Joon Ha} and Kim, {In Hye} and Cho, {Jeong Hwi} and Lee, {Jae Chul} and Koo, {Hyun Mo} and Gak Hwangbo and Yoo, {Ki Yeon} and Lee, {Choong Hyun} and Hwang, {In Koo} and Cho, {Jun Hwi} and Choi, {Soo Young} and Kwon, {Young Guen} and Kim, {Young Myeong} and Kang, {Il Jun} and Won, {Moo Ho}",
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Ahn, JH, Choi, JH, Park, JH, Kim, IH, Cho, JH, Lee, JC, Koo, HM, Hwangbo, G, Yoo, KY, Lee, CH, Hwang, IK, Cho, JH, Choi, SY, Kwon, YG, Kim, YM, Kang, IJ & Won, MH 2016, 'Long-Term Exercise Improves Memory Deficits via Restoration of Myelin and Microvessel Damage, and Enhancement of Neurogenesis in the Aged Gerbil Hippocampus after Ischemic Stroke', Neurorehabilitation and Neural Repair, vol. 30, no. 9, pp. 894-905. https://doi.org/10.1177/1545968316638444

Long-Term Exercise Improves Memory Deficits via Restoration of Myelin and Microvessel Damage, and Enhancement of Neurogenesis in the Aged Gerbil Hippocampus after Ischemic Stroke. / Ahn, Ji Hyeon; Choi, Jung Hoon; Park, Joon Ha; Kim, In Hye; Cho, Jeong Hwi; Lee, Jae Chul; Koo, Hyun Mo; Hwangbo, Gak; Yoo, Ki Yeon; Lee, Choong Hyun; Hwang, In Koo; Cho, Jun Hwi; Choi, Soo Young; Kwon, Young Guen; Kim, Young Myeong; Kang, Il Jun; Won, Moo Ho.

In: Neurorehabilitation and Neural Repair, Vol. 30, No. 9, 01.10.2016, p. 894-905.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Long-Term Exercise Improves Memory Deficits via Restoration of Myelin and Microvessel Damage, and Enhancement of Neurogenesis in the Aged Gerbil Hippocampus after Ischemic Stroke

AU - Ahn, Ji Hyeon

AU - Choi, Jung Hoon

AU - Park, Joon Ha

AU - Kim, In Hye

AU - Cho, Jeong Hwi

AU - Lee, Jae Chul

AU - Koo, Hyun Mo

AU - Hwangbo, Gak

AU - Yoo, Ki Yeon

AU - Lee, Choong Hyun

AU - Hwang, In Koo

AU - Cho, Jun Hwi

AU - Choi, Soo Young

AU - Kwon, Young Guen

AU - Kim, Young Myeong

AU - Kang, Il Jun

AU - Won, Moo Ho

PY - 2016/10/1

Y1 - 2016/10/1

N2 - Background. The positive correlation between therapeutic exercise and memory recovery in cases of ischemia has been extensively studied; however, long-term exercise begun after ischemic neuronal death as a chronic neurorestorative strategy has not yet been thoroughly examined. Objective. The purpose of this study is to investigate possible mechanisms by which exercise ameliorates ischemia-induced memory impairment in the aged gerbil hippocampus after transient cerebral ischemia. Methods. Treadmill exercise was begun 5 days after ischemia-reperfusion (I-R) and lasted for 1 or 4 weeks. The animals were sacrificed 31 days after the induction of ischemia. Changes in short-term memory, as well as the hippocampal expression of markers of cell proliferation, neuroblast differentiation, neurogenesis, myelin and microvessel repair, and growth factors were examined by immunohistochemistry and/or western blots. Results. Four weeks of exercise facilitated memory recovery despite neuronal damage in the stratum pyramidale (SP) of the hippocampal CA1 region and in the polymorphic layer (PoL) of the dentate gyrus (DG) after I-R. Long-term exercise enhanced cell proliferation and neuroblast differentiation in a time-dependent manner, and newly generated mature cells were found in the granule cell layer of the DG, but not in the SP of the CA1 region or in the PoL of the DG. In addition, long-term exercise ameliorated ischemia-induced damage of myelin and microvessels, which was correlated with increased BDNF expression in the CA1 region and the DG. Conclusions. These results suggest that long-term treadmill exercise after I-R can restore memory function through replacement of multiple damaged structures in the ischemic aged hippocampus.

AB - Background. The positive correlation between therapeutic exercise and memory recovery in cases of ischemia has been extensively studied; however, long-term exercise begun after ischemic neuronal death as a chronic neurorestorative strategy has not yet been thoroughly examined. Objective. The purpose of this study is to investigate possible mechanisms by which exercise ameliorates ischemia-induced memory impairment in the aged gerbil hippocampus after transient cerebral ischemia. Methods. Treadmill exercise was begun 5 days after ischemia-reperfusion (I-R) and lasted for 1 or 4 weeks. The animals were sacrificed 31 days after the induction of ischemia. Changes in short-term memory, as well as the hippocampal expression of markers of cell proliferation, neuroblast differentiation, neurogenesis, myelin and microvessel repair, and growth factors were examined by immunohistochemistry and/or western blots. Results. Four weeks of exercise facilitated memory recovery despite neuronal damage in the stratum pyramidale (SP) of the hippocampal CA1 region and in the polymorphic layer (PoL) of the dentate gyrus (DG) after I-R. Long-term exercise enhanced cell proliferation and neuroblast differentiation in a time-dependent manner, and newly generated mature cells were found in the granule cell layer of the DG, but not in the SP of the CA1 region or in the PoL of the DG. In addition, long-term exercise ameliorated ischemia-induced damage of myelin and microvessels, which was correlated with increased BDNF expression in the CA1 region and the DG. Conclusions. These results suggest that long-term treadmill exercise after I-R can restore memory function through replacement of multiple damaged structures in the ischemic aged hippocampus.

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