Leptin levels in patients with Parkinson's disease: A systematic review and meta-analysis

Rahnemayan, Sama; Mirghafourvand, Mojgan; Fathalizadeh, Arezoo; Faramarzi, Elnaz; Reyhanifard, Anita; Mahmoodpoor, Ata; Sanaie, Sarvin

doi:10.1016/j.clnesp.2020.11.001

Cited by 9 publications

(5 citation statements)

References 43 publications

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“…Accumulating in vivo and in vitro studies have suggested that leptin has notable effects on neuroprotection (Bahor et al., 2017; Begley & Ellis, 2012; Fernandez‐Martos et al., 2017; Liu et al., 2020; Marwarha et al., 2010) as well as on improving learning and cognitive function in Alzheimer´s disease (AD) (Farr et al., 2006; Sato et al., 2011; Searcy et al., 2012). Many of the neurological beneficial properties of leptin are currently being experimentally probed in order to get a strong foothold of the therapeutic implications for other neurological disorders as Parkinson's disease (Rahnemayan et al., 2021; Zou et al., 2019). In the context of ALS, leptin levels are inversely associated with ALS risk (Nagel et al., 2017).…”

Section: Introductionmentioning

confidence: 99%

The potential benefit of leptin therapy against amyotrophic lateral sclerosis (ALS)

et al. 2021

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Background Targeting leptin could represent a rational strategy to treat amyotrophic lateral sclerosis (ALS), as previously clinical studies have shown its levels to be associated with a lower risk of ALS disease. However, very little is known about the potential influence of leptin in altering disease progression in ALS, as it has thus far been correlated with the protection exerted by increased fat mass stores. Methods We studied the impact of leptin treatment beginning at 42‐days of age (asymptomatic stage of disease) in the TDP‐43 (TDP43A315T) transgenic (Tg) ALS mouse model. Results Our study shows that leptin treatment was associated with altered expression of adipokines and metabolic proteins in TDP43A315T mice. We also observed that weight loss decline was less prominent after leptin treatment in TDP43A315T mice relative to vehicle‐treated animals. In TDP43A315T mice treated with leptin the disease duration lasted longer along with an improvement in motor performance relative to vehicle‐treated animals. Conclusions Collectively, our results support leptin as a potential novel treatment approach for ALS.

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Section: Introductionmentioning

confidence: 99%

The potential benefit of leptin therapy against amyotrophic lateral sclerosis (ALS)

et al. 2021

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“…Decreased dynamic control of ghrelin has been demonstrated at prodromal stages, prompting the question of whether this is an early symptomatic change or causative mechanism (129) . Although conflicting results for leptin levels have been published in recent years, a recent meta-analysis suggested that this remains normal (130) . Evidence exists for a role of mitochondrial dysfunction in the aetiology of PD (131) , suggesting that an intrinsic dysfunction of energy handling may exist in affected individuals, with neuronal cells particularly sensitive to abnormalities of cellular respiration.…”

Section: Metabolic Homoeostasismentioning

confidence: 99%

Parkinson's disease: the nutrition perspective

et al. 2021

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Parkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease and affects about 1% of the population over the age of 60 years in industrialised countries. The aim of this review is to examine nutrition in PD across three domains: dietary intake and the development of PD; whole body metabolism in PD and the effects of PD symptoms and treatment on nutritional status. In most cases, PD is believed to be caused by a combination of genetic and environmental factors and although there has been much research in the area, evidence suggests that poor dietary intake is not a risk factor for the development of PD. The evidence about body weight changes in both the prodromal and symptomatic phases of PD is inconclusive and is confounded by many factors. Malnutrition in PD has been documented as has sarcopaenia, although the prevalence of the latter remains uncertain due to a lack of consensus in the definition of sarcopaenia. PD symptoms, including those which are gastrointestinal and non-gastrointestinal, are known to adversely affect nutritional status. Similarly, PD treatments can cause nausea, vomiting and constipation, all of which can adversely affect nutritional status. Given that the prevalence of PD will increase as the population ages, it is important to understand the interplay between PD, comorbidities and nutritional status. Further research may contribute to the development of interventional strategies to improve symptoms, augment care and importantly, enhance the quality of life for patients living with this complex neurodegenerative disease.

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“…Notably, a recent meta-analysis, including only 198 PD patients and 182 controls, found that the serum leptin levels in PD patients were slightly lower compared to those in the control group, although the difference did not reach statistical significance. 596 These limited findings emphasize the need for more comprehensive research to understand the mechanisms and functions of leptin in the onset, progression, and management of PD.…”

Section: Ghrelinmentioning

confidence: 99%

Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases

Loh,

Mak,

Tan

et al. 2024

Sig Transduct Target Ther

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The human gastrointestinal tract is populated with a diverse microbial community. The vast genetic and metabolic potential of the gut microbiome underpins its ubiquity in nearly every aspect of human biology, including health maintenance, development, aging, and disease. The advent of new sequencing technologies and culture-independent methods has allowed researchers to move beyond correlative studies toward mechanistic explorations to shed light on microbiome–host interactions. Evidence has unveiled the bidirectional communication between the gut microbiome and the central nervous system, referred to as the “microbiota–gut–brain axis”. The microbiota–gut–brain axis represents an important regulator of glial functions, making it an actionable target to ameliorate the development and progression of neurodegenerative diseases. In this review, we discuss the mechanisms of the microbiota–gut–brain axis in neurodegenerative diseases. As the gut microbiome provides essential cues to microglia, astrocytes, and oligodendrocytes, we examine the communications between gut microbiota and these glial cells during healthy states and neurodegenerative diseases. Subsequently, we discuss the mechanisms of the microbiota–gut–brain axis in neurodegenerative diseases using a metabolite-centric approach, while also examining the role of gut microbiota-related neurotransmitters and gut hormones. Next, we examine the potential of targeting the intestinal barrier, blood–brain barrier, meninges, and peripheral immune system to counteract glial dysfunction in neurodegeneration. Finally, we conclude by assessing the pre-clinical and clinical evidence of probiotics, prebiotics, and fecal microbiota transplantation in neurodegenerative diseases. A thorough comprehension of the microbiota–gut–brain axis will foster the development of effective therapeutic interventions for the management of neurodegenerative diseases.

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Leptin levels in patients with Parkinson's disease: A systematic review and meta-analysis

Cited by 9 publications

References 43 publications

The potential benefit of leptin therapy against amyotrophic lateral sclerosis (ALS)

The potential benefit of leptin therapy against amyotrophic lateral sclerosis (ALS)

Parkinson's disease: the nutrition perspective

Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases

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