Free carnitine and branched chain amino acids are not good biomarkers in Huntington’s disease

Castilhos, Raphael Machado; Augustin, Marina Coutinho; Santos, João Batista Oliveira dos; Pedroso, José Luiz; Barsottini, Orlando Graziani Póvoas; Saba, Roberta Arb; Ferraz, Henrique Ballalai; Vargas, Fernando; Furtado, Gabriel Vasata; Polese-Bonatto, Márcia; Rodrigues, Luiza Paulsen; Sena, Lucas Schenatto; Vargas, Carmen Regla; Saraiva-Pereira, Maria Luiza; Jardim, Laura Bannach; Neurogenética, Rede

doi:10.1590/0004-282x20190152

Cited by 2 publications

(1 citation statement)

References 15 publications

(26 reference statements)

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“…Genetically it is associated with the expansion of cytosine adenine guanine trinucleotide repeats in the Huntingtin gene [ 41 , 42 ]. There is no treatment available for the management of HD, although in pre-clinical studies several flavonoids have shown promising protective effects against HD, e.g., hesperidin and naringin in a rat model of HD [ 43 ]. Other studies conducted on quercetin, rutin, and myricetin have also reduced the symptoms of HD in animal models of the disease [ 44 , 45 ].…”

Section: Flavonoids and Neuroprotectionmentioning

confidence: 99%

Antioxidant and Anti-Inflammatory Effects of Citrus Flavonoid Hesperetin: Special Focus on Neurological Disorders

et al. 2020

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Neurodegenerative disorders have emerged as a serious health issue in the current era. The most common neurodegenerative disorders are Alzheimer’s disease (AD), Parkinson’s disease, multiple sclerosis, and amyotrophic lateral sclerosis (ALS). These diseases involve progressive impairment of neurodegeneration and memory impairment. A wide range of compounds have been identified as potential neuroprotective agents against different models of neurodegeneration both in vivo and in vitro. Hesperetin, a flavanone class of citrus flavonoid, is a derivative of hesperidin found in citrus fruits such as oranges, grapes, and lemons. It has been extensively reported that hesperetin exerts neuroprotective effects in experimental models of neurodegenerative diseases. In this systematic review, we have compiled all the studies conducted on hesperetin in both in vivo and in vitro models of neurodegeneration. Here, we have used an approach to lessen the bias in each study, providing a least biased, broad understanding of findings and impartial conclusions of the strength of evidence and the reliability of findings. In this review, we collected different papers from a wide range of journals describing the beneficial effects of hesperetin on animal models of neurodegeneration. Our results demonstrated consistent neuroprotective effects of hesperetin against different models of neurodegeneration. In addition, we have summarized its underlying mechanisms. This study provides the foundations for future studies and recommendations of further mechanistic approaches to conduct preclinical studies on hesperetin in different models.

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Section: Flavonoids and Neuroprotectionmentioning

confidence: 99%

Antioxidant and Anti-Inflammatory Effects of Citrus Flavonoid Hesperetin: Special Focus on Neurological Disorders

et al. 2020

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The microbiota–gut–brain axis in Huntington's disease: pathogenic mechanisms and therapeutic targets

Ekwudo,

Gubert,

Hannan

2024

The FEBS Journal

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Huntington's disease (HD) is a currently incurable neurogenerative disorder and is typically characterized by progressive movement disorder (including chorea), cognitive deficits (culminating in dementia), psychiatric abnormalities (the most common of which is depression), and peripheral symptoms (including gastrointestinal dysfunction). There are currently no approved disease‐modifying therapies available for HD, with death usually occurring approximately 10–25 years after onset, but some therapies hold promising potential. HD subjects are often burdened by chronic diarrhea, constipation, esophageal and gastric inflammation, and a susceptibility to diabetes. Our understanding of the microbiota–gut–brain axis in HD is in its infancy and growing evidence from preclinical and clinical studies suggests a role of gut microbial population imbalance (gut dysbiosis) in HD pathophysiology. The gut and the brain can communicate through the enteric nervous system, immune system, vagus nerve, and microbiota‐derived‐metabolites including short‐chain fatty acids, bile acids, and branched‐chain amino acids. This review summarizes supporting evidence demonstrating the alterations in bacterial and fungal composition that may be associated with HD. We focus on mechanisms through which gut dysbiosis may compromise brain and gut health, thus triggering neuroinflammatory responses, and further highlight outcomes of attempts to modulate the gut microbiota as promising therapeutic strategies for HD. Ultimately, we discuss the dearth of data and the need for more longitudinal and translational studies in this nascent field. We suggest future directions to improve our understanding of the association between gut microbes and the pathogenesis of HD, and other ‘brain and body disorders’.

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Free carnitine and branched chain amino acids are not good biomarkers in Huntington’s disease

Cited by 2 publications

References 15 publications

Antioxidant and Anti-Inflammatory Effects of Citrus Flavonoid Hesperetin: Special Focus on Neurological Disorders

Antioxidant and Anti-Inflammatory Effects of Citrus Flavonoid Hesperetin: Special Focus on Neurological Disorders

The microbiota–gut–brain axis in Huntington's disease: pathogenic mechanisms and therapeutic targets

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