TY - JOUR
T1 - Microtubules, schizophrenia and cognitive behavior
T2 - Preclinical development of davunetide (NAP) as a peptide-drug candidate
AU - Gozes, Illana
N1 - Funding Information:
I am indebted to my colleagues mentioned in the manuscript for their dedicated work. Support was provided by Allon Therapeutics Inc., A.M.N. Foundation and Canadian Friends of Tel Aviv University (CFTAU). Professor Gozes is the incumbent of the Lily and Avraham Gildor Chair for the Investigation of Growth Factors, and the Director of the Adams Super Center for Brain Studies, the Levie-Edersheim-Gitter Institute for Functional Brain Imaging and the Dr. Diana and Zelman Elton (Elbaum) Laboratory for Molecular Neuroendocrinology.
PY - 2011/2
Y1 - 2011/2
N2 - NAP (davunetide) is an active fragment of activity-dependent neuroprotective protein (ADNP). ADNP and the homologous protein ADNP2 provide cell protection. ADNP is essential for brain formation, proper development and neuronal plasticity, all reported to be impaired in schizophrenia. ADNP haploinsufficiecy inhibits social and cognitive functions, major hallmarks in schizophrenia. Imbalance in ADNP/ADNP2 expression in the schizophrenia brain may impact disease progression. NAP treatment partly ameliorates ADNP haploinsufficiecy. The microtubule, stable tubule-only polypeptide (STOP)-deficient mice were shown to provide a reliable model for schizophrenia. Daily intranasal NAP treatment significantly decreased hyperactivity in STOP-deficient mice and protected visual memory, supporting further clinical development.
AB - NAP (davunetide) is an active fragment of activity-dependent neuroprotective protein (ADNP). ADNP and the homologous protein ADNP2 provide cell protection. ADNP is essential for brain formation, proper development and neuronal plasticity, all reported to be impaired in schizophrenia. ADNP haploinsufficiecy inhibits social and cognitive functions, major hallmarks in schizophrenia. Imbalance in ADNP/ADNP2 expression in the schizophrenia brain may impact disease progression. NAP treatment partly ameliorates ADNP haploinsufficiecy. The microtubule, stable tubule-only polypeptide (STOP)-deficient mice were shown to provide a reliable model for schizophrenia. Daily intranasal NAP treatment significantly decreased hyperactivity in STOP-deficient mice and protected visual memory, supporting further clinical development.
KW - ADNP2
KW - Activity-dependent neuroprotective protein (ADNP)
KW - Hyperactivity
KW - NAP (davunetide)
KW - Schizophrenia
KW - Stable tubule-only polypeptide (STOP)
KW - Tau
KW - Visual memory
UR - http://www.scopus.com/inward/record.url?scp=78751646734&partnerID=8YFLogxK
U2 - 10.1016/j.peptides.2010.10.030
DO - 10.1016/j.peptides.2010.10.030
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AN - SCOPUS:78751646734
SN - 0196-9781
VL - 32
SP - 428
EP - 431
JO - Peptides
JF - Peptides
IS - 2
ER -