New insights into metabolism dysregulation after TBI DOI Creative Commons
Helena Oft, Dennis Simon,

Dandan Sun

и другие.

Journal of Neuroinflammation, Год журнала: 2024, Номер 21(1)

Опубликована: Июль 29, 2024

Abstract Traumatic brain injury (TBI) remains a leading cause of death and disability that places great physical, social, financial burden on individuals the health system. In this review, we summarize new research into metabolic changes described in clinical TBI trials, some which have already shown promise for informing classification staging. We focus our discussion derangements glucose metabolism, cell respiration/mitochondrial function to ketone lipid metabolism/oxidation emphasize potentially novel biomarkers outcome prediction intervention offer insights possible underlying mechanisms from preclinical pathology. Finally, discuss nutrition supplementation studies aim harness gut/microbiome-brain connection manipulate systemic/cellular metabolism improve post-TBI recovery. Taken together, narrative review summarizes published TBI-associated highlighting potential metabolite use, cellular processes linking these markers pathology as well limitations future considerations “omics” work.

Язык: Английский

Astrocyte energy and neurotransmitter metabolism in Alzheimer’s disease: Integration of the glutamate/GABA-glutamine cycle DOI
Jens V. Andersen, Arne Schousboe, Alexei Verkhratsky

и другие.

Progress in Neurobiology, Год журнала: 2022, Номер 217, С. 102331 - 102331

Опубликована: Июль 21, 2022

Язык: Английский

Процитировано

151

Altered glucose metabolism in Alzheimer's disease: Role of mitochondrial dysfunction and oxidative stress DOI
Saikat Dewanjee, Pratik Chakraborty, Hiranmoy Bhattacharya

и другие.

Free Radical Biology and Medicine, Год журнала: 2022, Номер 193, С. 134 - 157

Опубликована: Окт. 4, 2022

Язык: Английский

Процитировано

127

The metabolic costs of cognition DOI
Sharna D. Jamadar, Anna Behler, Hamish A Deery

и другие.

Trends in Cognitive Sciences, Год журнала: 2025, Номер unknown

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

2

Metabolic disorders on cognitive dysfunction after traumatic brain injury DOI Creative Commons
Jinqing Lai, Yan‐Chuan Shi, Shu Lin

и другие.

Trends in Endocrinology and Metabolism, Год журнала: 2022, Номер 33(7), С. 451 - 462

Опубликована: Май 7, 2022

Cognitive dysfunction is a common adverse consequence of traumatic brain injury (TBI). After injury, the and other organs trigger series complex metabolic changes, including reduced glucose metabolism, enhanced lipid peroxidation, disordered neurotransmitter secretion, imbalanced trace element synthesis. In recent years, several research clinical studies have demonstrated that metabolism directly or indirectly affects cognitive after TBI, but mechanisms remain unclear. Drugs improve symptoms caused by TBI are under investigation treatments target processes expected to function in future. This review explores impact disorders on provides new strategies for treatment disorders.

Язык: Английский

Процитировано

54

A High-Sugar Diet Consumption, Metabolism and Health Impacts with a Focus on the Development of Substance Use Disorder: A Narrative Review DOI Open Access
Kacper Witek,

Karolina Wydra,

Małgorzata Filip

и другие.

Nutrients, Год журнала: 2022, Номер 14(14), С. 2940 - 2940

Опубликована: Июль 18, 2022

Carbohydrates are important macronutrients in human and rodent diet patterns that play a key role crucial metabolic pathways provide the necessary energy for proper body functioning. Sugar homeostasis intake require complex hormonal nervous control to balance. Added sugar processed food results metabolic, cardiovascular, disorders. Epidemiological reports have shown enhanced consumption of sweet products children adults, especially reproductive age pregnant women, which can lead susceptibility offspring's health diseases early life or adulthood proneness mental In this review, we discuss impacts high-sugar (HSD) during perinatal and/or postnatal periods on neural behavioural disturbances as well development substance use disorder (SUD). Since several emotional recognized predictors SUD, also present how HSD enhances impulsive behaviour, stress, anxiety depression. Apart from influence these mood disturbances, added render addiction. Both addictive substances change sensitivity brain rewarding neurotransmission signalling. The collected studies could be assessing intake, via maternal dietary patterns, clinical perspective SUD prevention pre-existing Methodology: This narrative review focuses roles foods glucose fructose (SUD) drugs abuse. literature was reviewed by two authors independently according topic review. We searched PubMed Scopus databases Multidisciplinary Digital Publishing Institute open access scientific journals using following keyword search strategy depending theme chapter: "high-sugar diet" OR "high-carbohydrate "sugar" "glucose" "fructose" "added sugar" AND keywords. excluded inaccessible pay-walled articles, abstracts, conference papers, editorials, letters, commentary, short notes. Reviews, experimental studies, epidemiological data, published since 1990s, were chapter structure. After search, all duplicates thrown out full texts read, findings rescreened. selection process, appropriate papers included

Язык: Английский

Процитировано

47

Neuroprotection and Disease Modification by Astrocytes and Microglia in Parkinson Disease DOI Creative Commons
Shinichi Takahashi,

Kyoko Mashima

Antioxidants, Год журнала: 2022, Номер 11(1), С. 170 - 170

Опубликована: Янв. 17, 2022

Oxidative stress and neuroinflammation are common bases for disease onset progression in many neurodegenerative diseases. In Parkinson disease, which is characterized by the degeneration of dopaminergic neurons resulting dopamine depletion, pathogenesis differs between hereditary solitary forms often unclear. addition to pathogenicity alpha-synuclein as a pathological marker, involvement itself its interactions with glial cells (astrocyte or microglia) have attracted attention. Pacemaking activity, hallmark neurons, essential homeostatic maintenance adequate concentrations synaptic cleft, but it imposes burden on mitochondrial oxidative glucose metabolism, leading reactive oxygen species production. Astrocytes provide endogenous neuroprotection brain producing releasing antioxidants response stress. Additionally, protective function astrocytes can be modified microglia. Some types microglia themselves thought exacerbate pro-inflammatory factors (M1 microglia). Although these inflammatory may further trigger conversion astrocytes, induce astrocytic neuroprotective effects (A2 astrocytes) simultaneously. Interestingly, both express receptors, upregulated presence neuroinflammation. The anti-inflammatory receptor stimulation also attracting attention because functions greatly affected depletion therapeutic replacement disease. this review article, we will focus antioxidative their synergism dopamine.

Язык: Английский

Процитировано

43

Mitochondrial heterogeneity in diseases DOI Creative Commons
Long Chen,

Mengnan Zhou,

Hao Li

и другие.

Signal Transduction and Targeted Therapy, Год журнала: 2023, Номер 8(1)

Опубликована: Авг. 23, 2023

Abstract As key organelles involved in cellular metabolism, mitochondria frequently undergo adaptive changes morphology, components and functions response to various environmental stresses demands. Previous studies of research have gradually evolved, from focusing on morphological change analysis systematic multiomics, thereby revealing the mitochondrial variation between cells or within population a single cell. The phenomenon features is defined as heterogeneity. Moreover, heterogeneity has been reported influence variety physiological processes, including tissue homeostasis, repair, immunoregulation, tumor progression. Here, we comprehensively review different tissues under pathological states, involving variant DNA, RNA, protein lipid components. Then, mechanisms that contribute are also summarized, such mutation genome import proteins result DNA Additionally, multiple perspectives investigated better comprehend mysteries cells. Finally, summarize prospective heterogeneity-targeting therapies terms alleviating oxidative damage, reducing carbon stress enhancing biogenesis relieve conditions. possibility recent technological advances targeted gene editing discussed.

Язык: Английский

Процитировано

31

miR-129-5p as a biomarker for pathology and cognitive decline in Alzheimer’s disease DOI Creative Commons
Sang‐Won Han, Jung‐Min Pyun, Paula J. Bice

и другие.

Alzheimer s Research & Therapy, Год журнала: 2024, Номер 16(1)

Опубликована: Янв. 9, 2024

Abstract Background Alzheimer’s dementia (AD) pathogenesis involves complex mechanisms, including microRNA (miRNA) dysregulation. Integrative network and machine learning analysis of miRNA can provide insights into AD pathology prognostic/diagnostic biomarkers. Methods We performed co-expression to identify modules associated with AD, its neuropathology markers, cognition using brain tissue profiles from the Religious Orders Study Rush Memory Aging Project (ROS/MAP) ( N = 702) as a discovery dataset. association hub miRNAs cognition. After selecting target genes miRNAs, we their then pathway-based enrichment analysis. For replication, consensus ROS/MAP dataset an independent 16) Gene Expression Omnibus (GEO). Furthermore, approach assess performance for classification. Results Network identified glucose metabolism pathway-enriched module (M3) significantly Five (miR-129-5p, miR-433, miR-1260, miR-200a, miR-221) M3 had significant associations clinical and/or pathologic traits, miR129-5p by far strongest across all phenotypes. Gene-set corresponding enriched biological pathways ErbB, AMPK, MAPK, mTOR signaling pathways. Consensus two AD-associated (miR-129-5p miR-221). Machine showed that classification (area under curve (AUC) 0.807) age, sex, APOE ε4 carrier status was improved 6.3% inclusion five miRNAs. Conclusions signatures, especially miR-129-5p, cognition, enhancing our understanding leading better potential diagnostic/prognostic

Язык: Английский

Процитировано

10

Cordycepin Modulates Microglial M2 Polarization Coupled with Mitochondrial Metabolic Reprogramming by Targeting HKII and PDK2 DOI Creative Commons
Xin Zhong, Shiqiang Gong,

Linghui Meng

и другие.

Advanced Science, Год журнала: 2024, Номер 11(31)

Опубликована: Июнь 18, 2024

Abstract The microenvironment mediated by the microglia (MG) M1/M2 phenotypic switch plays a decisive role in neuronal fate and cognitive function of Alzheimer's disease (AD). However, impact metabolic reprogramming on microglial polarization its underlying mechanism remains elusive. This study reveals that cordycepin improved memory APP/PS1 mice, as well attenuated damage triggering MG‐M2 characterized increased OXPHOS glycolysis, rather than directly protecting neurons. Simultaneously, partially alleviates mitochondrial induced inhibitors further promoting transformation increasing survival. Through confirmation distribution mitochondria via isolation followed HPLC‐MS/MS techniques, HKII PDK2 are identified potential targets cordycepin. By investigating effects inhibitors, through which targeted to elevate ECAR levels glycolysis pathway while targeting enhance OCR PDH‐mediated pathway, thereby inducing polarization, survival exerting an anti‐AD is elucidated.

Язык: Английский

Процитировано

10

Effects of ketogenic diet on cognitive function of patients with Alzheimer's disease: a systematic review and meta-analysis DOI Creative Commons
Liyang Rong, Yating Peng, Qi Shen

и другие.

The journal of nutrition health & aging, Год журнала: 2024, Номер 28(8), С. 100306 - 100306

Опубликована: Июнь 28, 2024

Ketogenic diets (KD) have shown remarkable effects in many disease areas. It has been demonstrated numerous animal experiments that KD is effective the treatment of Alzheimer's (AD). But clinical effect treating AD uncertain.

Язык: Английский

Процитировано

9