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Acylated Ghrelin as a Multi-Targeted Therapy for Alzheimer's and Parkinson's Disease
Open accessAbstract
Much thought has been given to the impact of Amyloid Beta, Tau and Alpha-Synuclein in the development of Alzheimer's disease (AD) and Parkinson's disease (PD), yet the clinical failures of the recent decades indicate that there are further pathological mechanisms at work. Indeed, besides amyloids, AD and PD are characterized by the culminative interplay of oxidative stress, mitochondrial dysfunction and hyperfission, defective autophagy and mitophagy, systemic inflammation, BBB and vascular damage, demyelination, cerebral insulin resistance, the loss of dopamine production in PD, impaired neurogenesis and, of course, widespread axonal, synaptic and neuronal degeneration that leads to cognitive and motor impediments. Interestingly, the acylated form of the hormone ghrelin has shown the potential to ameliorate the latter pathologic changes, although some studies indicate a few complications that need to be considered in the long-term administration of the hormone. As such, this review will illustrate the wide-ranging neuroprotective properties of acylated ghrelin and critically evaluate the hormone's therapeutic benefits for the treatment of AD and PD.
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![Figure 1 Illustration of the neuroprotective pathways following GHS-R1α activation by AG or ghrelin agonists in neurons and astrocytes. [1] Mitochondrial function: By activating the key mediator AMPK, AG induces the transcriptional co-activator PGC1α. The latter, in concert with NRF1/2, enhances mitochondrial biogenesis, the synthesis of TFAM and TFAM-mediated mtDNA replication/transcription. By increasing the transcription of Mfn2, PGC1α protects from MPTP/rotenone-driven mitochondrial fragmentation. In addition, AMPK/GAPDH-mediated phosphorylation of nuclear SIRT1 frees the latter deacetylase and leads to the inactivation of pro-inflammatory NF-κB, the activation of the Bax-sequestrating Ku70 and the stimulation of FoxO1-regulated anti-oxidant and autophagy genes. Lastly, the induction of the AMPK/CPT1a/UCP2 pathway prevents pathological mitochondrial depolarization (such as by Aβ). Furthermore, UCP2-driven mitochondrial uncoupling increases the mitochondrial respiration, bioenergetic efficiency and mitigates the co-generation of ROS by the ETC, which may protect from the stress-induced hyperproduction of ATP and ROS during early stages of AD. Given that more advanced stages of AD are characterized by neuronal glucose hypometabolism and a chronic shift toward other bioenergetic processes, in particular the β-oxidation of lipids, AG may support the compensatory execution of β-oxidation to generate ATP. Notably, AMPK inhibits ACC, thus depleting the intracellular malonyl-CoA pools and, in turn, elevating the activity levels of the malonyl-CoA-regulated CPT1a (not shown). [2] Autophagy: (Macro)autophagy is primarily driven by the GHS-R1α/AMPK/TSC1/2-mediated inactivation of mTOR/mTORC1 and the direct phosphorylation of ULK1 via AMPK, resulting in the degradation of cellular waste, amyloids (Aβ/Tau/α-synuclein) and defective mitochondria. Moreover, by raising the intracellular NAD+ levels, AMPK reinforces its activity through the activation of the cytoplasmic, NAD+-dependent SIRT1 and the AMPK-kinase LKB1. SIRT1 is also involved in the deacetylation of Tau at Lys174, which was reported to abrogate the pathological propagation of Tau throughout the brain. Besides triggering autophagy, AG upregulates various ATGs and Beclin-1, while promoting autophagosome maturation and the autophagic flux. [3] Astrocytes: The stimulation of GHS-R1α encourages the expression of the lactate-efflux transporter MCT4 by astrocytes, leading to the increased secretion of lactate, a potent energy source for neurons.](/paper-figures/bb43b69c10a6471c92498c61434590b7/acylated-ghrelin-as-a-multi-targeted-therapy-for-alzheimer-s-and-parkinson-s-figure-1.jpg)
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“Moreover, the beneficial role of ghrelin in the central nervous system has been widely discussed, including enhanced cognition [48, 59–61].”
From Protective PLCG2 variants associate with a delayed onset of Alzheimer’s disease among heterozygous APOE ε4 carriers (2026) · cites this paper as [60]
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Cited by
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Self-citationAcetyl-CoA Metabolism and Histone Acetylation in the Regulation of Aging and Lifespan
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The protective PLCG2 variants delay Alzheimer's disease onset age in APOE ϵ4 carriersPreprint
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“This indicates its potential as a target for treating neurodegenerative disorders, including Parkinson’s and Alzheimer’s diseases [15] .”
Metadata
- Authors
- Reich, N., & Hölscher, C.
- Affiliations
- Lancaster University (GB)
- Henan University of Chinese Medicine (CN)
- Corresponding author
- Reich, Niklas
- Venue
- Frontiers in Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2020-12-14
- Volume
- 14
- Pages
- 614828-614828
- ISSN
- 1662-453X (ISSN-L)
- PMC
- PMC7767977
- OpenAlex
- W3111850577
- Cited by
- 48
- References
- 476
- Citations by year
- 2026: 7 · 2025: 6 · 2024: 7 · 2023: 9 · 2022: 13 · 2021: 6
- FWCI
- 0.92
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Lancaster EPrints (Lancaster University) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- acylated ghrelin, Alzheimer's disease, Parkinson's disease, neuroprotection, oxidative stress, mitochondrial dysfunction, autophagy, mitophagy, systemic inflammation, blood-brain barrier, dopamine depletion, neurogenesis, multi-target therapy
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