TY - JOUR
T1 - Neuroprotection against neurodegenerative diseases
T2 - Development of a novel hybrid neuroprotective peptide Colivelin
AU - Chiba, Tomohiro
AU - Nishimoto, Ikuo
AU - Aiso, Sadakazu
AU - Matsuoka, Masaaki
N1 - Funding Information:
We are indebted to Drs Yasuo Ikeda and Masaki Kitajima for essential help. We thank Drs. John T. Potts Jr., Etsuro Ogata, and Mr. Yoshiomi and Mrs. Yumi Tamai for indispensable support; Ms. Takako Hiraki and Ms. Tomo Yoshida-Nishimoto for essential cooperation; Dr. Dovie Wylie for expert assistance; and all members of the Departments of Anatomy for essential cooperation. This work was supported by in part by a grant from NOEVIR CO., LTD, Takeda Science Foundation, KEIO Gijuku Academic Development Funds (T.C.), and the Japan Society for the Promotion of Science.
PY - 2007/2
Y1 - 2007/2
N2 - Neuronal death is directly implicated in the pathogenesis of neurodegenerative diseases (NDDs). NDDs cannot be cured because the mechanisms underlying neuronal death are too complicated to be therapeutically suppressed. Neuroprotective factors, such as neurotrophins, certain growth factors, neurotrophic cytokines, and short neuroprotective peptides, support neuronal survival in both physiological and pathological conditions, suggesting that these factors may be good drug candidates for NDDs. We recently generated a novel neuroprotective peptide named Colivelin by attaching activity-dependent neurotrophic factor (ADNF) to the N-terminus of a potent Humanin derivative, AGA-(C8R)HNG17. HN was originally identified from an Alzheimer's disease (AD) brain as an endogenous neuroprotective peptide that suppresses ADrelevant toxicity. Colivelin protects neurons from death relevant to NDDs by activating two independent prosurvival signals: an ADNF-mediated Ca2+/calmodulin-dependent protein kinase IV pathway and an HN-mediated STAT3 pathway. The neuroprotective effect of Colivelin provides novel insights into therapy for NDDs.
AB - Neuronal death is directly implicated in the pathogenesis of neurodegenerative diseases (NDDs). NDDs cannot be cured because the mechanisms underlying neuronal death are too complicated to be therapeutically suppressed. Neuroprotective factors, such as neurotrophins, certain growth factors, neurotrophic cytokines, and short neuroprotective peptides, support neuronal survival in both physiological and pathological conditions, suggesting that these factors may be good drug candidates for NDDs. We recently generated a novel neuroprotective peptide named Colivelin by attaching activity-dependent neurotrophic factor (ADNF) to the N-terminus of a potent Humanin derivative, AGA-(C8R)HNG17. HN was originally identified from an Alzheimer's disease (AD) brain as an endogenous neuroprotective peptide that suppresses ADrelevant toxicity. Colivelin protects neurons from death relevant to NDDs by activating two independent prosurvival signals: an ADNF-mediated Ca2+/calmodulin-dependent protein kinase IV pathway and an HN-mediated STAT3 pathway. The neuroprotective effect of Colivelin provides novel insights into therapy for NDDs.
KW - ADNF
KW - Colivelin
KW - Humanin
KW - Neurodegenerative diseases
KW - Neuronal death
KW - Neuroprotection
UR - https://www.scopus.com/pages/publications/34347357647
UR - https://www.scopus.com/pages/publications/34347357647#tab=citedBy
U2 - 10.1007/BF02700624
DO - 10.1007/BF02700624
M3 - Article
C2 - 17519506
AN - SCOPUS:34347357647
SN - 0893-7648
VL - 35
SP - 55
EP - 84
JO - Molecular Neurobiology
JF - Molecular Neurobiology
IS - 1
ER -