Antiserum to activity-dependent neurotrophic factor produces neuronal cell death in CNS cultures: immunological and biological specificity

Gozes, Illana; Davidson, Ariane; Gozes, Yehoshua; Mascolo, Richard; Barth, Rolf N.; Warren, Dale; Hauser, Janet; Brenneman, Douglas E.

doi:10.1016/s0165-3806(96)00215-5

Cited by 51 publications

(45 citation statements)

References 38 publications

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“…ADNP was found to share a structural and immunological motif with activity-dependent neurotrophic factor (ADNF), which was shown to exhibit femtomolar neuroprotection in cell culture [9,10,26,27]. The shortest active site of ADNF has been identified and synthesized as the short peptide ADNF-9 (single letter code: SALLRSIPA) [28].…”

Section: Neuroprotective Peptidesmentioning

confidence: 99%

Neurotrophic Effects of the Peptide NAP: A Novel Neuroprotective Drug Candidate

Gozes

Spivak-Pohis²

2006

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This short review outlines the scientific progression from the neuropeptide vasoactive intestinal peptide as a neuroprotective agent that acts through glial cells to increase and modulate the synthesis and secretion of novel neuroprotective substances. Recent development in the studies on activity-dependent neuroprotective protein (ADNP) and activity-dependent neurotrophic factor (ADNF) and short peptide derivatives of these proteins, ADNF-9 and NAP suggest that these peptides are neurotrophic and promote neurite outgrowth. These short peptides hold promise in future neuroprotective/neurotrophic drug development. Clinical development of NAP is currently in progress by Allon Therapeutics, Inc.

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Section: Neuroprotective Peptidesmentioning

confidence: 99%

Neurotrophic Effects of the Peptide NAP: A Novel Neuroprotective Drug Candidate

Gozes

Spivak-Pohis²

2006

CAR

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“…Antibody studies suggested that ADNF-like immunoreactivity is important for brain wellbeing [19] and that ADNF-like molecules mediate VIP neuroprotective and neurotrophic activities [9,12,20,21]. Preparation of ADNF-9 like analogues resulted in the discovery of neuroprotective activity in an all D-amino acids ADNF-9 (D-SAL, D-Ser-D-Ala-D-Leu-D-LeuDArg-D-Ser-D-Ile-D-Pro-D-Ala) suggesting a non-chiral mode of action [22].…”

Section: Introductionmentioning

confidence: 99%

Protection Against Tauopathy by the Drug Candidates NAP (Davunetide) and D-SAL: Biochemical, Cellular and Behavioral Aspects

Shiryaev¹,

Pikman²,

Giladi³

et al. 2011

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Activity-dependent neuroprotective protein (ADNP) is essential for brain formation and partial deficiency in ADNP results in cognitive deficits coupled with tauopathy and neuronal cell death. Our previous results indicated that a peptide snippet from ADNP, NAPVSIPQ (NAP, generic name, davunetide) can restore in part ADNP deficiencies. NAP interacts with tubulin and this interaction is displaced by the NAP related peptide that is derived from activity-dependent neurotrophic factor (ADNF), SALLRSIPA (SAL) and its all D-amino acid peptide derivative (D-SAL, also known as AL-309). Both NAP and D-SAL were shown to protect neurons against amyloid beta toxicity however the mechanism of protection is still under investigation. In addition, NAP protects against tau hyperphosphorylation associated with ADNP deficiency, in vivo. To investigate whether the mechanism of in vitro neuroprotection relates to the in vivo protection against tauopathy and to draw potential additional parallelism between NAP and D-SAL, we asked if: 1]NAP and D-SAL protect against amyloid beta related tau hyperphosphorylation in vitro; and 2] D-SAL protects against haploinsufficiency in ADNP, inhibiting tauopathy in vivo. Assessment of NAP and D-SAL neuroprotection in primary cortical neuro-glial cultures treated with amyloid beta showed that both peptides reduced toxin-related neuronal damage and protected against tau hyperphosphorylation. In vivo, chronic D-SAL administration protected against tau hyperphosphorylation associated with ADNP deficiency (ADNP+/- mice), showing for the first time protection against deficits in odor discrimination and in social recognition. These studies associate neuroprotection in vivo and in vitro and provide a broad base for future drug development based on NAP and D-SAL against multiple neurodegenerative conditions.

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“…VIP treatment of astrocytes produced an increase in ADNP mRNA (Bassan et al, 1999) and the secretion of growth factors (e.g., ADNF, activity-dependent neurotrophic factor) (Brenneman and Gozes, 1996). ADNP and ADNF share a short peptide motif: NAPVSIPQ (NAP) in ADNP and SALLRSIPA (ADNF-9) in ADNF, which exhibit immunological similarity and femtomolar neuroprotection in cell culture (Gozes et al, 1997b;Brenneman et al, 1998;Bassan et al, 1999). NAP rescued rat cerebral cortical neurons from death associated with a wide range of neurotoxic agents, including the ␤-amyloid peptide and N-methyl-D-aspartate, NMDA (Bassan et al, 1999).…”

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confidence: 99%