Neuronal Cell Death in Alzheimers Disease and a Neuroprotective Factor, Humanin
Open accessAbstract
Brain atrophy caused by neuronal loss is a prominent pathological feature of Alzheimer's disease (AD). Amyloid beta (Abeta), the major component of senile plaques, is considered to play a central role in neuronal cell death. In addition to removal of the toxic Abeta, direct suppression of neuronal loss is an essential part of AD treatment; however, no such neuroprotective therapies have been developed. Excess amount of Abeta evokes multiple cytotoxic mechanisms, involving increase of the intracellular Ca(2+) level, oxidative stress, and receptor-mediated activation of cell-death cascades. Such diversity in cytotoxic mechanisms induced by Abeta clearly indicates a complex nature of the AD-related neuronal cell death. We have identified a 24-residue peptide, Humanin (HN), which suppresses in vitro neuronal cell death caused by all AD-related insults, including Abeta, so far tested. The anti-AD effect of HN has been further confirmed in vivo using mice with Abeta-induced amnesia. Altogether, such potent neuroprotective activity of HN against AD-relevant cytotoxicity both in vitro and in vivo suggests the potential clinical applications of HN in novel AD therapies aimed at controlling neuronal death.
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Aβ aggregates have neurotoxic effects causing neuron death in the presence of Aβ aggregates.
“Thus, our 3D models demonstrated that neurotoxic effects of Aβ aggregates, which is consistent with previous reports that Aβ aggregates contribute to the neuron death in AD brain.42”
From Acoustofluidic assembly of 3D neurospheroids to model Alzheimer's disease (2020) · cites this paper as [42]
Potential neuroprotective mechanisms fixate on inhibiting deleterious intraneuronal pathways triggered by toxic stimuli and amyloid-beta via interaction with neuronal targets.
“Potential neuroprotective mechanisms fixate on inhibiting deleterious intraneuronal pathways triggered by toxic stimuli and Aβ via the interaction with neuronal targets [36].”
From The Multifaceted Role of Neuroprotective Plants in Alzheimer’s Disease Treatment (2022) · cites this paper as [36]
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References 94 · Cited by 184
- Authors
- Niikura, T., Tajima, H., & Kita, Y.
- Affiliations
- Keio University (JP)
- Corresponding author
- Kita, Yoshiko
- ORCID
- Niikura, Takako
- Venue
- Current Neuropharmacology
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2006-04-01
- Volume
- 4
- Issue
- 2
- Pages
- 139-147
- ISSN
- 1570-159X (ISSN-L)
- PMC
- PMC2430668
- OpenAlex
- W1993249718
- Cited by
- 184
- References
- 94
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 14 · 2023: 24 · 2022: 36 · 2021: 21 · 2020: 14 · 2019: 6 · 2018: 12 · 2017: 5 · 2016: 4 · 2015: 4 · 2014: 4 · 2013: 5 · 2012: 4
- FWCI
- 1.77
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Current Neuropharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Japan Society for the Promotion of Science
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- Alzheimer's disease, neuronal cell death, humanin, neuroprotection, amyloid-beta, amyloid plaques, brain atrophy, oxidative stress, intracellular calcium, cytotoxicity, amnesia, peptide therapy
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