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Metabolites
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Brain Metabolic Alterations in Neurodegenerative Diseases
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Brain Metabolic Alterations in Neurodegenerative Diseases

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 7717

Special Issue Editors

Dr. Luciene Bruno Vieira

E-Mail Website
Guest Editor
Department of Pharmacology, Universidade Federal de Minas Gerais, Instituto de Ciências Biológicas, Belo Horizonte, Brasil
Interests: central mechanisms of feeding; glutamatergic system; neu-roinflamation; neurotransmission
Dr. Fabíola Mara Ribeiro

E-Mail Website
Guest Editor
Department of Biochemistry, Universidade Federal de Minas Gerais, Instituto de Ciências Biológicas, Belo Horizonte, Brasil
Interests: neurodegeneration; Huntigton´s disease; neurodegenerative diseases; neurotransmission

Special Issue Information

Dear Colleagues,

We are excited to announce a forthcoming Special Issue of Metabolites, entitled "Brain Metabolic Alterations in Neurodegenerative Diseases". Brain metabolic alterations are a common feature in neurodegenerative diseases, encompassing disrupted glucose metabolism, mitochondrial dysfunction, and neuroinflammation—all culminating in metabolic stress, which contributes to the progression and severity of these conditions. This issue will explore the intricate connections between hypometabolism, mitochondrial dysfunction, and metabolic changes in the context of neurodegenerative diseases. Understanding the complex relationship between metabolism and neurodegeneration is essential for the development of novel therapeutic interventions aimed at slowing or altering the course of these devastating disorders. Notably, this Special Issue welcomes the submission of not only basic research but also clinical studies, promoting a comprehensive exploration of this critical subject. Also, we aim to present cutting-edge reviews and original research articles that investigate the progression of metabolic alterations potentially implicated in neurodegenerative diseases.

Dr. Luciene Bruno Vieira
Dr. Fabíola Mara Ribeiro
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • glucose metabolism
  • mitochondrial dysfunction
  • neuroinflammation
  • neurodegeneration

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Published Papers (2 papers)

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Review

15 pages, 662 KiB  
Review
Unravelling Shared Pathways Linking Metabolic Syndrome, Mild Cognitive Impairment, Dementia, and Sarcopenia
by Daniela Ceccarelli Ceccarelli and Sebastiano Bruno Solerte
Metabolites 2025, 15(3), 159; https://doi.org/10.3390/metabo15030159 - 27 Feb 2025
Viewed by 1656
Abstract
Background: Aging is characterized by shared cellular and molecular processes, and aging-related diseases might co-exist in a cluster of comorbidities, particularly in vulnerable individuals whose phenotype meets the criteria for frailty. Whilst the multidimensional definition of frailty is still controversial, there is [...] Read more.
Background: Aging is characterized by shared cellular and molecular processes, and aging-related diseases might co-exist in a cluster of comorbidities, particularly in vulnerable individuals whose phenotype meets the criteria for frailty. Whilst the multidimensional definition of frailty is still controversial, there is an increasing understanding of the common pathways linking metabolic syndrome, cognitive decline, and sarcopenia, frequent conditions in frail elderly patients. Methods: We performed a systematic search in the electronic databases Cochrane Library and PubMed and included preclinical studies, cohort and observational studies, and trials. Discussion: Metabolic syndrome markers, such as insulin resistance and the triglyceride/HDL C ratio, correlate with early cognitive impairment. Insulin resistance is a cause of synaptic dysfunction and neurodegeneration. Conversely, fasting and fasting-mimicking agents promote neuronal resilience by enhancing mitochondrial efficiency, autophagy, and neurogenesis. Proteins acting as cellular metabolic sensors, such as SIRT1, play a pivotal role in aging, neuroprotection, and metabolic health. In AD, β-amyloid accumulation and hyperphosphorylated tau in neurofibrillary tangles can cause metabolic reprogramming in brain cells, shifting from oxidative phosphorylation to aerobic glycolysis, similar to the Warburg effect in cancer. The interrelation of metabolic syndrome, sarcopenia, and cognitive decline suggests that targeting these shared metabolic pathways could mitigate all the conditions. Pharmacological interventions, including GLP-1 receptor agonists, metformin, and SIRT 1 inducers, demonstrated neuroprotective effects in animals and some preliminary clinical models. Conclusions: These findings encourage further research on the prevention and treatment of neurodegenerative diseases as well as the drug-repurposing potential of molecules currently approved for diabetes, dyslipidemia, and metabolic syndrome. Full article
(This article belongs to the Special Issue Brain Metabolic Alterations in Neurodegenerative Diseases)
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22 pages, 1467 KiB  
Review
A Potential Role for the Ketogenic Diet in Alzheimer’s Disease Treatment: Exploring Pre-Clinical and Clinical Evidence
by Tadeu P. D. Oliveira, Ana L. B. Morais, Pedro L. B. dos Reis, András Palotás and Luciene B. Vieira
Metabolites 2024, 14(1), 25; https://doi.org/10.3390/metabo14010025 - 29 Dec 2023
Cited by 4 | Viewed by 5351
Abstract
Given the remarkable progress in global health and overall quality of life, the significant rise in life expectancy has become intertwined with the surging occurrence of neurodegenerative disorders (NDs). This emerging trend is poised to pose a substantial challenge to the fields of [...] Read more.
Given the remarkable progress in global health and overall quality of life, the significant rise in life expectancy has become intertwined with the surging occurrence of neurodegenerative disorders (NDs). This emerging trend is poised to pose a substantial challenge to the fields of medicine and public health in the years ahead. In this context, Alzheimer’s disease (AD) is regarded as an ND that causes recent memory loss, motor impairment and cognitive deficits. AD is the most common cause of dementia in the elderly and its development is linked to multifactorial interactions between the environment, genetics, aging and lifestyle. The pathological hallmarks in AD are the accumulation of β-amyloid peptide (Aβ), the hyperphosphorylation of tau protein, neurotoxic events and impaired glucose metabolism. Due to pharmacological limitations and in view of the prevailing glycemic hypometabolism, the ketogenic diet (KD) emerges as a promising non-pharmacological possibility for managing AD, an approach that has already demonstrated efficacy in addressing other disorders, notably epilepsy. The KD consists of a food regimen in which carbohydrate intake is discouraged at the expense of increased lipid consumption, inducing metabolic ketosis whereby the main source of energy becomes ketone bodies instead of glucose. Thus, under these dietary conditions, neuronal death via lack of energy would be decreased, inasmuch as the metabolism of lipids is not impaired in AD. In this way, the clinical picture of patients with AD would potentially improve via the slowing down of symptoms and delaying of the progression of the disease. Hence, this review aims to explore the rationale behind utilizing the KD in AD treatment while emphasizing the metabolic interplay between the KD and the improvement of AD indicators, drawing insights from both preclinical and clinical investigations. Via a comprehensive examination of the studies detailed in this review, it is evident that the KD emerges as a promising alternative for managing AD. Moreover, its efficacy is notably enhanced when dietary composition is modified, thereby opening up innovative avenues for decreasing the progression of AD. Full article
(This article belongs to the Special Issue Brain Metabolic Alterations in Neurodegenerative Diseases)
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