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A Sensitized IGF1 Treatment Restores Corticospinal Axon-Dependent Functions.

Abstract A major hurdle for functional recovery after both spinal cord injury and cortical stroke is the limited regrowth of the axons in the corticospinal tract (CST) that originate in the motor cortex and innervate the spinal cord. Despite recent advances in engaging the intrinsic mechanisms that control CST regrowth, it remains to be tested whether such methods can promote functional recovery in translatable settings. Here we show that post-lesional AAV-assisted co-expression of two soluble proteins, namely insulin-like growth factor 1 (IGF1) and osteopontin (OPN), in cortical neurons leads to robust CST regrowth and the recovery of CST-dependent behavioral performance after both T10 lateral spinal hemisection and a unilateral cortical stroke. In these mice, a compound able to increase axon conduction, 4-aminopyridine-3-methanol, promotes further improvement in CST-dependent behavioral tasks. Thus, our results demonstrate a potentially translatable strategy for restoring cortical dependent function after injury in the adult.
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Authors

Mayor MeshTerms
Keywords

4-aminopyridine

IGF1

axon regeneration

axon sprouting

ischemic stroke

osteopontin

spinal cord injury

Journal Title neuron
Publication Year Start




PMID- 28817801
OWN - NLM
STAT- In-Process
DA  - 20170817
LR  - 20170817
IS  - 1097-4199 (Electronic)
IS  - 0896-6273 (Linking)
VI  - 95
IP  - 4
DP  - 2017 Aug 16
TI  - A Sensitized IGF1 Treatment Restores Corticospinal Axon-Dependent Functions.
PG  - 817-833.e4
LID - S0896-6273(17)30685-2 [pii]
LID - 10.1016/j.neuron.2017.07.037 [doi]
AB  - A major hurdle for functional recovery after both spinal cord injury and cortical
      stroke is the limited regrowth of the axons in the corticospinal tract (CST) that
      originate in the motor cortex and innervate the spinal cord. Despite recent
      advances in engaging the intrinsic mechanisms that control CST regrowth, it
      remains to be tested whether such methods can promote functional recovery in
      translatable settings. Here we show that post-lesional AAV-assisted co-expression
      of two soluble proteins, namely insulin-like growth factor 1 (IGF1) and
      osteopontin (OPN), in cortical neurons leads to robust CST regrowth and the
      recovery of CST-dependent behavioral performance after both T10 lateral spinal
      hemisection and a unilateral cortical stroke. In these mice, a compound able to
      increase axon conduction, 4-aminopyridine-3-methanol, promotes further
      improvement in CST-dependent behavioral tasks. Thus, our results demonstrate a
      potentially translatable strategy for restoring cortical dependent function after
      injury in the adult.
CI  - Copyright (c) 2017 Elsevier Inc. All rights reserved.
FAU - Liu, Yuanyuan
AU  - Liu Y
AD  - F.M. Kirby Neurobiology Center, Boston Children's Hospital, 300 Longwood Avenue, 
      Boston, MA 02115, USA; Department of Neurology, Harvard Medical School, 300
      Longwood Avenue, Boston, MA 02115, USA.
FAU - Wang, Xuhua
AU  - Wang X
AD  - F.M. Kirby Neurobiology Center, Boston Children's Hospital, 300 Longwood Avenue, 
      Boston, MA 02115, USA; Department of Neurology, Harvard Medical School, 300
      Longwood Avenue, Boston, MA 02115, USA.
FAU - Li, Wenlei
AU  - Li W
AD  - F.M. Kirby Neurobiology Center, Boston Children's Hospital, 300 Longwood Avenue, 
      Boston, MA 02115, USA; Department of Neurology, Harvard Medical School, 300
      Longwood Avenue, Boston, MA 02115, USA; Department of Neurology, Affiliated
      Hospital of Nanjing University of Chinese Medicine, Nanjing 210004, China.
FAU - Zhang, Qian
AU  - Zhang Q
AD  - F.M. Kirby Neurobiology Center, Boston Children's Hospital, 300 Longwood Avenue, 
      Boston, MA 02115, USA; Department of Neurology, Harvard Medical School, 300
      Longwood Avenue, Boston, MA 02115, USA; Department of Neurobiology and
      Collaborative Innovation Center for Brain Science, Fourth Military Medical
      University, Xi'an 710032, China.
FAU - Li, Yi
AU  - Li Y
AD  - F.M. Kirby Neurobiology Center, Boston Children's Hospital, 300 Longwood Avenue, 
      Boston, MA 02115, USA; Department of Neurology, Harvard Medical School, 300
      Longwood Avenue, Boston, MA 02115, USA.
FAU - Zhang, Zicong
AU  - Zhang Z
AD  - F.M. Kirby Neurobiology Center, Boston Children's Hospital, 300 Longwood Avenue, 
      Boston, MA 02115, USA; Department of Neurology, Harvard Medical School, 300
      Longwood Avenue, Boston, MA 02115, USA.
FAU - Zhu, Junjie
AU  - Zhu J
AD  - F.M. Kirby Neurobiology Center, Boston Children's Hospital, 300 Longwood Avenue, 
      Boston, MA 02115, USA; Department of Neurology, Harvard Medical School, 300
      Longwood Avenue, Boston, MA 02115, USA.
FAU - Chen, Bo
AU  - Chen B
AD  - F.M. Kirby Neurobiology Center, Boston Children's Hospital, 300 Longwood Avenue, 
      Boston, MA 02115, USA; Department of Neurology, Harvard Medical School, 300
      Longwood Avenue, Boston, MA 02115, USA.
FAU - Williams, Philip R
AU  - Williams PR
AD  - F.M. Kirby Neurobiology Center, Boston Children's Hospital, 300 Longwood Avenue, 
      Boston, MA 02115, USA; Department of Neurology, Harvard Medical School, 300
      Longwood Avenue, Boston, MA 02115, USA.
FAU - Zhang, Yiming
AU  - Zhang Y
AD  - F.M. Kirby Neurobiology Center, Boston Children's Hospital, 300 Longwood Avenue, 
      Boston, MA 02115, USA; Department of Neurology, Harvard Medical School, 300
      Longwood Avenue, Boston, MA 02115, USA.
FAU - Yu, Bin
AU  - Yu B
AD  - Department of Neurobiology and Collaborative Innovation Center for Brain Science,
      Fourth Military Medical University, Xi'an 710032, China.
FAU - Gu, Xiaosong
AU  - Gu X
AD  - Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education,
      Co-innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu
      226001, China.
FAU - He, Zhigang
AU  - He Z
AD  - F.M. Kirby Neurobiology Center, Boston Children's Hospital, 300 Longwood Avenue, 
      Boston, MA 02115, USA; Department of Neurology, Harvard Medical School, 300
      Longwood Avenue, Boston, MA 02115, USA. Electronic address:
      [email protected]
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Neuron
JT  - Neuron
JID - 8809320
OTO - NOTNLM
OT  - 4-aminopyridine
OT  - IGF1
OT  - axon regeneration
OT  - axon sprouting
OT  - ischemic stroke
OT  - osteopontin
OT  - spinal cord injury
EDAT- 2017/08/18 06:00
MHDA- 2017/08/18 06:00
CRDT- 2017/08/18 06:00
PHST- 2017/02/21 [received]
PHST- 2017/05/23 [revised]
PHST- 2017/07/28 [accepted]
AID - S0896-6273(17)30685-2 [pii]
AID - 10.1016/j.neuron.2017.07.037 [doi]
PST - ppublish
SO  - Neuron. 2017 Aug 16;95(4):817-833.e4. doi: 10.1016/j.neuron.2017.07.037.