Tau and caspase 3 as targets for neuroprotection.

Idan-Feldman A, Ostritsky R, Gozes I

International journal of Alzheimer's disease30 May 2012Cited by 27 (Europe PMC)

PMID22693678PMCIDPMC3369463DOI10.1155/2012/493670PepBankPUB-22693678

Summary

The peptide drug candidate NAP (davunetide) has demonstrated protective effects in various in vivo and in vitro models of neurodegeneration. NAP was shown to reduce tau hyperphosphorylation as well as to prevent caspase-3 activation and cytochrome-3 release from mitochondria, both characteristic of apoptotic cell death. Recent studies suggest that caspases may play a role in tau pathology. The purpose of this study was to evaluate the effect of NAP on tau hyperphosphorylation and caspase activity in the same biological system. Our experimental setup used primary neuronal cultures subjected to oxygen-glucose deprivation (OGD), with and without NAP or caspase inhibitor. Cell viability was assessed by measuring mitochondrial activity (MTS assay), and immunoblots were used for analyzing protein level. It was shown that apoptosis was responsible for all cell death occurring following ischemia, and NAP treatment showed a concentration-dependent protection from cell death. Ischemia caused an increase in the levels of active caspase-3 and hyperphosphorylated tau, both of which were prevented by either NAP or caspase-inhibitor treatment. Our data suggest that, in this model system, caspase activation may be an upstream event to tau hyperphosphorylation, although additional studies will be required to fully elucidate the cascade of events.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

3 results from studies that gave the peptide. No result from this study comes from people.

01LabIn vitro (cells)Efficacy outcome
In primary neuronal cultures after ischemia, NAP provided concentration-dependent protection from cell death.
In plain wordsIn cells, NAP reduced death after oxygen-glucose deprivation compared with no NAP, with a concentration-dependent response.
Peptide
Davunetide
Outcome
DecreaseCell death
Study
n: not reported in source
primary neuronal cultures subjected to oxygen-glucose deprivation
Comparator
Oxygen-glucose deprivation without NAP
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
It was shown that apoptosis was responsible for all cell death occurring following ischemia, and NAP treatment showed a concentration-dependent protection from cell death.
2 context sentences(design, population, supporting numbers)
Summary · context
Our experimental setup used primary neuronal cultures subjected to oxygen-glucose deprivation (OGD), with and without NAP or caspase inhibitor.
Summary · context
Cell viability was assessed by measuring mitochondrial activity (MTS assay), and immunoblots were used for analyzing protein level.
Show in the study text Report a problemFND-2269367801
02LabIn vitro (cells)Mechanism
In primary neuronal cultures, NAP prevented the ischemia-induced increase in active caspase-3.
In plain wordsIn cells, NAP prevented increased active caspase-3 after oxygen-glucose deprivation compared with no NAP.
Peptide
Davunetide
Outcome
DecreaseActive caspase-3
Study
n: not reported in source
primary neuronal cultures subjected to oxygen-glucose deprivation
Comparator
Oxygen-glucose deprivation without NAP
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Ischemia caused an increase in the levels of active caspase-3 and hyperphosphorylated tau, both of which were prevented by either NAP or caspase-inhibitor treatment.
2 context sentences(design, population, supporting numbers)
Summary · context
Our experimental setup used primary neuronal cultures subjected to oxygen-glucose deprivation (OGD), with and without NAP or caspase inhibitor.
Summary · context
Cell viability was assessed by measuring mitochondrial activity (MTS assay), and immunoblots were used for analyzing protein level.
Show in the study text Report a problemFND-2269367802
03LabIn vitro (cells)Mechanism
In primary neuronal cultures, NAP prevented the ischemia-induced increase in hyperphosphorylated tau.
In plain wordsIn cells, NAP prevented increased abnormal tau phosphorylation after oxygen-glucose deprivation compared with no NAP.
Peptide
Davunetide
Outcome
DecreaseHyperphosphorylated tau
Study
n: not reported in source
primary neuronal cultures subjected to oxygen-glucose deprivation
Comparator
Oxygen-glucose deprivation without NAP
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Ischemia caused an increase in the levels of active caspase-3 and hyperphosphorylated tau, both of which were prevented by either NAP or caspase-inhibitor treatment.
2 context sentences(design, population, supporting numbers)
Summary · context
Our experimental setup used primary neuronal cultures subjected to oxygen-glucose deprivation (OGD), with and without NAP or caspase inhibitor.
Summary · context
Cell viability was assessed by measuring mitochondrial activity (MTS assay), and immunoblots were used for analyzing protein level.
Show in the study text Report a problemFND-2269367803

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
27 Oct 2026, 18:20 UTC
Study results updated
Version 1
27 Oct 2026, 16:32 UTC
First added · source update from Europe PMC

Subjects

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Publication types

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