The Neuronal Actions of Leptin and the Implications for Treating Alzheimer’s Disease
Open accessAbstract
It is widely accepted that the endocrine hormone leptin controls food intake and energy homeostasis via activation of leptin receptors expressed on hypothalamic arcuate neurons. The hippocampal formation also displays raised levels of leptin receptor expression and accumulating evidence indicates that leptin has a significant impact on hippocampal synaptic function. Thus, cellular and behavioural studies support a cognitive enhancing role for leptin as excitatory synaptic transmission, synaptic plasticity and glutamate receptor trafficking at hippocampal Schaffer collateral (SC)-CA1 synapses are regulated by leptin, and treatment with leptin enhances performance in hippocampus-dependent memory tasks. Recent studies indicate that hippocampal temporoammonic (TA)-CA1 synapses are also a key target for leptin. The ability of leptin to regulate TA-CA1 synapses has important functional consequences as TA-CA1 synapses are implicated in spatial and episodic memory processes. Moreover, degeneration is initiated in the TA pathway at very early stages of Alzheimer’s disease, and recent clinical evidence has revealed links between plasma leptin levels and the incidence of Alzheimer’s disease (AD). Additionally, accumulating evidence indicates that leptin has neuroprotective actions in various AD models, whereas dysfunctions in the leptin system accelerate AD pathogenesis. Here, we review the data implicating the leptin system as a potential novel target for AD, and the evidence that boosting the hippocampal actions of leptin may be beneficial.
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Leptin counteracts Aβ pathology and tau phosphorylation to prevent synaptic dysfunction.
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Diet-induced obesity alters memory consolidation in female rats
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Neurotrophic effects of leptin on cerebellar Purkinje but not granule neurons in vitro
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Self-citationProtective effects of leptin against cerebral ischemia/reperfusion injury (Review)
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Self-citationMetabolic abnormalities and hypoleptinemia in α-synuclein A53T mutant mice
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Correction: Hyperleptinemia in children with autosomal recessive spinal muscular atrophy type I-III
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Elmquist (1998) · doi:10.1002/(sici)1096-9861(19980615)395:4
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Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases
Loh, J. S., Mak, W. Q., Tan, L. K. S., Ng, C. X., Chan, H. H., Yeow, S. H., Foo, J. B., Ong, Y. S., How, C. W., & Khaw, K. Y. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01743-1 · Cited by 1,193 · see citing works
- Authors
- Hamilton, K., & Harvey, J.
- Affiliations
- University of Dundee (GB)
- Corresponding author
- Harvey, Jenni
- Venue
- Pharmaceuticals
- Publisher
- MDPI AG
- Published
- 2021-01-11
- Volume
- 14
- Issue
- 1
- Pages
- 52
- ISSN
- 1424-8247 (ISSN-L)
- PMC
- PMC7827292
- OpenAlex
- W3119567578
- Cited by
- 36
- References
- 103
- Citations by year
- 2026: 1 · 2025: 8 · 2024: 9 · 2023: 9 · 2022: 6 · 2021: 3
- FWCI
- 0.93
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Pharmaceuticals (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Discovery Research Portal (University of Dundee) (acceptedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Alzheimer's Society (449 (AS-PhD-18-007).)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- leptin, Alzheimer's disease, hippocampus, leptin receptor, synaptic plasticity, glutamate receptor trafficking, Schaffer collateral-CA1 synapses, memory, neuroprotection, energy homeostasis, plasma leptin, therapeutic target
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