A Novel, Multi-Faceted Perception of Lactate in Neurology

Mason, Shayne

doi:10.3389/fnins.2020.00460

Cited by 9 publications

(8 citation statements)

References 46 publications

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“…In pediatric tuberculosis, cerebrospinal fluid (CSF) lactate is increased concomitantly with a decrease in glucose [75]. The authors hypothesize that astrocytes augment the secretion of lactate which can be utilized by microglia as an energy source for the production of ROS to destroy the invading Mycobacterium tuberculosis [76].…”

Section: Microglial Lactate Metabolism In Infections and Brain Injuriesmentioning

confidence: 99%

Microglial metabolic flexibility: emerging roles for lactate

Monsorno

Buckinx

Paolicelli

2022

Trends in Endocrinology & Metabolism

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Section: Microglial Lactate Metabolism In Infections and Brain Injuriesmentioning

confidence: 99%

Microglial metabolic flexibility: emerging roles for lactate

Monsorno

Buckinx

Paolicelli

2022

Trends in Endocrinology & Metabolism

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“…The reported neuroprotective potential of lactate, for example in traumatic brain injury (reviewed by [115]) or in ischemia [116], and their possible anti-inflammatory effects [93], may contradict the assumption of a detrimental role of lactate in PD pathogenesis. However, toxic effects of high levels of lactate have been reported in models in which low levels were neuroprotective (e.g., [116]).…”

Section: The Interplay Between Hypoxia Acidification and Inflammationmentioning

confidence: 99%

Hypoxia, Acidification and Inflammation: Partners in Crime in Parkinson’s Disease Pathogenesis?

Burtscher

Millet

2021

Immuno

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Like in other neurodegenerative diseases, protein aggregation, mitochondrial dysfunction, oxidative stress and neuroinflammation are hallmarks of Parkinson’s disease (PD). Differentiating characteristics of PD include the central role of α-synuclein in the aggregation pathology, a distinct vulnerability of the striato-nigral system with the related motor symptoms, as well as specific mitochondrial deficits. Which molecular alterations cause neurodegeneration and drive PD pathogenesis is poorly understood. Here, we summarize evidence of the involvement of three interdependent factors in PD and suggest that their interplay is likely a trigger and/or aggravator of PD-related neurodegeneration: hypoxia, acidification and inflammation. We aim to integrate the existing knowledge on the well-established role of inflammation and immunity, the emerging interest in the contribution of hypoxic insults and the rather neglected effects of brain acidification in PD pathogenesis. Their tight association as an important aspect of the disease merits detailed investigation. Consequences of related injuries are discussed in the context of aging and the interaction of different brain cell types, in particular with regard to potential consequences on the vulnerability of dopaminergic neurons in the substantia nigra. A special focus is put on the identification of current knowledge gaps and we emphasize the importance of related insights from other research fields, such as cancer research and immunometabolism, for neurodegeneration research. The highlighted interplay of hypoxia, acidification and inflammation is likely also of relevance for other neurodegenerative diseases, despite disease-specific biochemical and metabolic alterations.

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“…Using the online search criteria of "tuberculous meningitis" and "metabolomics" in PubMed, up to the end of 2020, yielded 14 hits; of these, 11 studies [19][20][21][22][23][24][25][26][27][28][29] contained metabolic information on TBM in CSF from humans, and are discussed in this review. Further examination of these 11 studies yielded three more CSF metabolomics studies on TBM [30][31][32].…”

Section: Literature Search Parametersmentioning

confidence: 99%

“…Indeed, it is true that lactic acid can be produced by anaerobic respiration-pyruvate is converted to lactate, catalyzed by lactate dehydrogenase and the oxidation of NADH to NAD + . However, the true metabolic role(s) of CSF lactate have just begun to emerge [24], with increasing evidence supporting the notion that CSF lactate has a novel, multifaceted perception in neurology [26]. One of the new roles proposed for CSF lactate in TBM cases is the astrocyte-microglia lactate shuttle (AMLS).…”

Section: Csf Lactatementioning

confidence: 99%

CSF Metabolomics of Tuberculous Meningitis: A Review

Mason

Solomons

2021

Metabolites

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From the World Health Organization’s global TB report for 2020, it is estimated that in 2019 at least 80,000 children (a particularly vulnerable population) developed tuberculous meningitis (TBM)—an invariably fatal disease if untreated—although this is likely an underestimate. As our latest technologies have evolved—with the unprecedented development of the various “omics” disciplines—a mountain of new data on infectious diseases have been created. However, our knowledge and understanding of infectious diseases are still trying to keep pace. Metabolites offer much biological information, but the insights they permit can be difficult to derive. This review summarizes current metabolomics studies on cerebrospinal fluid (CSF) from TBM cases and collates the metabolic data reported. Collectively, CSF metabolomics studies have identified five classes of metabolites that characterize TBM: amino acids, organic acids, nucleotides, carbohydrates, and “other”. Taken holistically, the information given in this review serves to promote the mechanistic action of hypothesis generation that will drive and direct future studies on TBM.

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A Novel, Multi-Faceted Perception of Lactate in Neurology

Cited by 9 publications

References 46 publications

Microglial metabolic flexibility: emerging roles for lactate

Microglial metabolic flexibility: emerging roles for lactate

Hypoxia, Acidification and Inflammation: Partners in Crime in Parkinson’s Disease Pathogenesis?

CSF Metabolomics of Tuberculous Meningitis: A Review

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