Targeting midkine and pleiotrophin signalling pathways in addiction and neurodegenerative disorders: recent progress and perspectives
Open accessAbstract
Midkine (MK) and pleiotrophin (PTN) are two neurotrophic factors that are highly up‐regulated in different brain regions after the administration of various drugs of abuse and in degenerative areas of the brain. A deficiency in both MK and PTN has been suggested to be an important genetic factor, which confers vulnerability to the development of the neurodegenerative disorders associated with drugs of abuse in humans. In this review, evidence demonstrating that MK and PTN limit the rewarding effects of drugs of abuse and, potentially, prevent drug relapse is compiled. There is also convincing evidence that MK and PTN have neuroprotective effects against the neurotoxicity and development of neurodegenerative disorders induced by drugs of abuse. Exogenous administration of MK and/or PTN into the CNS by means of non‐invasive methods is proposed as a novel therapeutic strategy for addictive and neurodegenerative diseases. Identification of new molecular targets downstream of the MK and PTN signalling pathways or pharmacological modulation of those already known may also provide a more traditional, but probably effective, therapeutic strategy for treating addictive and neurodegenerative disorders. Linked Articles: This article is part of a themed section on Midkine. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue‐4
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Midkine is highly correlated with Aβ in human cases and in 5xFAD mice and is proposed to antagonize Aβ cytotoxicity.
“Midkine is also highly correlated with Aβ in human cases and in the 5xFAD mice and it is proposed to antagonize Aβ cytotoxicity (Herradon and Perez-Garcia, 2014).”
From Deep Multilayer Brain Proteomics Identifies Molecular Networks in Alzheimer’s Disease Progression (2020) · cites this paper as Herradon and Perez-Garcia, 2014
The Alzheimer's disease discussion (indexed under “Drug addiction”; page unavailable) reports midkine in nearly all amyloid-β plaques examined in eight patients and says it inhibits amyloid-β cytotoxicity. It also describes greater plaque deposition in mice lacking midkine, but does not identify those mice as 5xFAD or report a high correlation in that model. (LLM, conf=0.88)
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Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration
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Research works printed but not linked: 3
- Ichihara-Tanaka K, Oohira A, Rumsby M, Muramatsu T (2006). Neuroglycan C is a novel midkine receptor involved in process elongation of oligodendroglial precursor-like cells. J Biol Chem 281: 30857-30864.
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Deep Multilayer Brain Proteomics Identifies Molecular Networks in Alzheimer’s Disease Progression
Bai, B., Wang, X., Li, Y., Chen, P.-C., Yu, K., Dey, K. K., Yarbro, J. M., Han, X., Lutz, B. M., Rao, S., et al. (2020) · Neuron · doi:10.1016/j.neuron.2019.12.015 · Cited by 632 · see citing works
“Midkine is also highly correlated with Aβ in human cases and in the 5xFAD mice and it is proposed to antagonize Aβ cytotoxicity (Herradon and Perez-Garcia, 2014).”
BackgroundPleiotrophin: Activity and mechanism
(2020) · Advances in Clinical Chemistry · doi:10.1016/bs.acc.2020.02.003 · Cited by 98 · see citing works
- Authors
- Herradón, G., & Pérez‐García, C.
- Affiliations
- Universidad San Pablo CEU (ES)
- Corresponding author
- Herradón, G
- Venue
- British Journal of Pharmacology
- Publisher
- Wiley
- Published
- 2014-01-24
- Volume
- 171
- Issue
- 4
- Pages
- 837-848
- ISSN
- 0007-1188 (ISSN-L)
- 1476-5381
- PMC
- PMC3925022
- OpenAlex
- W1572674029
- Cited by
- 88
- References
- 2
- Citations by year
- 2026: 4 · 2025: 10 · 2024: 8 · 2023: 8 · 2022: 5 · 2021: 5 · 2020: 12 · 2019: 5 · 2018: 4 · 2017: 7 · 2016: 6 · 2015: 8 · 2014: 6
- FWCI
- 0.68
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- British Journal of Pharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministerio de Ciencia e Innovación of Spain (SAF2007-61528, SAF2009-08136)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pharmacological Receptor Mechanisms and Effects
- Keywords
- midkine, pleiotrophin, neurotrophic factors, addiction, drugs of abuse, neurodegenerative diseases, drug reward, drug relapse, neuroprotection, neurotoxicity, gene deficiency, therapeutic target
- MeSH terms
- Midkine, Animals, Carrier Proteins, Humans, Nerve Growth Factors, Signal Transduction, Cytokines, Neurodegenerative Diseases, Substance-Related Disorders
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