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Cited by 211Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

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Role of p38/MAPKs in Alzheimer's Disease: Implications for Amyloid Beta Toxicity Targeted Therapy

Kheiri, Ghazaleh, Dolatshahi, Mahsa, Rahmani, Farzaneh, Rezaei, Nima·2018·Reviews in the Neurosciences
DOI 10.1515/revneuro-2018-0008
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Abstract

A myriad of environmental and genetic factors, as well as the physiologic process of aging, contribute to Alzheimer's disease (AD) pathology. Neuroinflammation is and has been a focus of interest, as a common gateway for initiation of many of the underlying pathologies of AD. Amyloid beta (Aβ) toxicity, increasing RAGE expression, tau hyperphosphorylation, induction of apoptosis, and deregulated autophagy are among other mechanisms, partly entangled and being explained by activation of mitogen-activated protein kinase (MAPK) and MAPK signaling. p38 MAPK is the most essential regulator of Aβ induced toxicity from this family. p38 induces NF-κB activation, glutamate excitotoxicity, and disruption of synaptic plasticity, which are other implications of all justifying the p38 MAPK as a potential target to break the vicious Aβ toxicity cycle. Until recently, many in vivo and in vitro studies have investigated the effects of p38 MAPK inhibitors in AD. The pyridinyl imidazole compounds SB202190 and SB203580 have shown promising anti-apoptotic results in vivo. MW108 inhibits activation of p38 and is able to postpone cognitive decline in animal models. The PD169316, with anti-inflammatory, anti-oxidative, and anti-apoptotic features, has improved spatial memory in vivo. Natural compounds from Camellia sinensis (green tea), polyphenols from olive oil, pinocembrin from propolis, and the puerarine extract isoflavones, have shown strong anti-apoptotic features, mediated by p38 MAPK inhibition. Use of these drug targets is limited due to central nervous system side effects or cross-reactivity with other kinases, predicting the low efficacy of these drugs in clinical trials.

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Metadata

Authors
Kheiri, G., Dolatshahi, M., Rahmani, F., & Rezaei, N.
Affiliations
Universal Scientific Education and Research Network (IR)
Corresponding author
Rezaei, Nima
ORCID
Venue
Reviews in the Neurosciences
Publisher
Walter de Gruyter GmbH
Published
2018-12-19
Volume
30
Issue
1
Pages
9-30
ISSN
  • 0334-1763 (ISSN-L)
  • 2191-0200
DOI
10.1515/revneuro-2018-0008
OpenAlex
W2804716129
Cited by
211
References
200
Citations by year
2026: 16 · 2025: 35 · 2024: 27 · 2023: 39 · 2022: 29 · 2021: 35 · 2020: 23 · 2019: 6 · 2018: 1
FWCI
2.30
Type
journal article
Language
en
Open access
closed
Locations
  • Reviews in the Neurosciences (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, p38 MAPK, amyloid-beta toxicity, MAPK signaling, neuroinflammation, NF-κB activation, glutamate excitotoxicity, synaptic plasticity, p38 inhibitor, SB202190, SB203580, PD169316, apoptosis, tau hyperphosphorylation, autophagy, green tea polyphenols, olive oil polyphenols, pinocembrin, puerarin, natural compounds, cognitive decline
MeSH terms
Receptor for Advanced Glycation End Products, Alzheimer Disease, Animals, Enzyme Inhibitors, Humans, Signal Transduction, Amyloid beta-Peptides, p38 Mitogen-Activated Protein Kinases

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