Brain-derived neurotrophic factor (BDNF) epigenomic modifications and brain-related phenotypes in humans: A systematic review

Treble‐Barna, Amery; Heinsberg, Lacey W.; Stec, Zachary; Breazeale, Stephen; Davis, Tara S.; Kesbhat, Aboli A.; Chattopadhyay, Ansuman; VonVille, Helena M.; Ketchum, Andrea; Yeates, Keith Owen; Kochanek, Patrick M.; Weeks, Daniel E.; Conley, Yvette P.

doi:10.1016/j.neubiorev.2023.105078

Cited by 13 publications

(11 citation statements)

References 244 publications

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“…Animal experiments demonstrated that SIRT1–BDNF signaling pathway activation improved the learning and memory function of vascular cognitive impairment rats ( 51 ). BDNF is a neurotrophin family member, a key factor in sympathetic nervous system development, and is known as the fertilizer of the brain ( 52 ). BDNF helps the brain generate new neural connections, repair damaged brain cells, and protect healthy brain cells ( 53 ).…”

Section: Discussionmentioning

confidence: 99%

Exploration of the SIRT1-mediated BDNF–TrkB signaling pathway in the mechanism of brain damage and learning and memory effects of fluorosis

Wang,

Li,

Tang

et al. 2023

Front. Public Health

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IntroductionFluoride is considered an environmental pollutant that seriously affects organisms and ecosystems, and its harmfulness is a perpetual public health concern. The toxic effects of fluoride include organelle damage, oxidative stress, cell cycle destruction, inflammatory factor secretion, apoptosis induction, and synaptic nerve transmission destruction. To reveal the mechanism of fluorosis-induced brain damage, we analyzed the molecular mechanism and learning and memory function of the SIRT1-mediated BDNF–TrkB signaling pathway cascade reaction in fluorosis-induced brain damage through in vivo experiments.MethodsThis study constructed rat models of drinking water fluorosis using 50 mg/L, 100 mg/L, and 150 mg/L fluoride, and observed the occurrence of dental fluorosis in the rats. Subsequently, we measured the fluoride content in rat blood, urine, and bones, and measured the rat learning and memory abilities. Furthermore, oxidative stress products, inflammatory factor levels, and acetylcholinesterase (AchE) and choline acetyltransferase (ChAT) activity were detected. The pathological structural changes to the rat bones and brain tissue were observed. The SIRT1, BDNF, TrkB, and apoptotic protein levels were determined using western blotting.ResultsAll rats in the fluoride exposure groups exhibited dental fluorosis; decreased learning and memory abilities; and higher urinary fluoride, bone fluoride, blood fluoride, oxidative stress product, and inflammatory factor levels compared to the control group. The fluoride-exposed rat brain tissue had abnormal AchE and ChAT activity, sparsely arranged hippocampal neurons, blurred cell boundaries, significantly fewer astrocytes, and swollen cells. Furthermore, the nucleoli were absent from the fluoride-exposed rat brain tissue, which also contained folded neuron membranes, deformed mitochondria, absent cristae, vacuole formation, and pyknotic and hyperchromatic chromatin. The fluoride exposure groups had lower SIRT1, BDNF, and TrkB protein levels and higher apoptotic protein levels than the control group, which were closely related to the fluoride dose. The findings demonstrated that excessive fluoride caused brain damage and affected learning and memory abilities.DiscussionCurrently, there is no effective treatment method for the tissue damage caused by fluorosis. Therefore, the effective method for preventing and treating fluorosis damage is to control fluoride intake.

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Section: Discussionmentioning

confidence: 99%

Exploration of the SIRT1-mediated BDNF–TrkB signaling pathway in the mechanism of brain damage and learning and memory effects of fluorosis

Wang,

Li,

Tang

et al. 2023

Front. Public Health

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“…Cognitive function is the complex interaction between brain neurons executed at the neural network level, while maintaining the balance of brain energy metabolism is one of the key factors to ensure cognitive ability . Neurons in the CNS, especially in the hypothalamus, play an important role in controlling energy balance . The hypothalamus is a key region for regulating animal feeding and energy balance, and BDNF and TrkB genes are expressed in various regions of the hypothalamus. , The BDNF signal of astrocytes regulates neuronal activity in the ventromedial hypothalamus in response to changes in energy state, and loss of BDNF signaling in the paraventricular hypothalamus leads to increased appetite, decreased motor activity, and severe obesity .…”

Section: Discussionmentioning

confidence: 99%

Hydroxytyrosol Alleviates Obesity-Induced Cognitive Decline by Modulating the Expression Levels of Brain-Derived Neurotrophic Factors and Inflammatory Factors in Mice

Liu,

Lu,

Tian

et al. 2024

J. Agric. Food Chem.

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Hydroxytyrosol (HT; 3,4-dihydroxyphenyl ethanol) is an important functional polyphenol in olive oil. Our study sought to evaluate the protective effects and underlying mechanisms of HT on obesity-induced cognitive impairment. A high-fat and high-fructose-diet-induced obese mice model was treated with HT for 14 weeks. The results show that HT improved the learning and memory abilities and enhanced the expressions of brain-derived neurotrophic factors (BDNFs) and postsynaptic density proteins, protecting neuronal and synaptic functions in obese mice. Transcriptomic results further confirmed that HT improved cognitive impairment by regulating gene expression in neural system development and synaptic function-related pathways. Moreover, HT treatment alleviated neuroinflammation in the brain of obese mice. To sum up, our results indicated that HT can alleviate obesity-induced cognitive dysfunction by enhancing BDNF expression and alleviating neuroinflammation in the brain, which also means that HT may become a potentially useful nutritional supplement to alleviate obesity-induced cognitive decline.

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“…That study strongly supports the development of DNAm biomarkers of TBI using easily accessible peripheral blood leukocytes, as well as a focus on BDNF. Finally, taking an approach that collects DNAm data across the genome has the added advantage of being able to adjust for cell type heterogeneity, reducing potential confounding related to cell type-phenotype associations, which can help provide a greater biological understanding of ABI [39].…”

Section: Bdnf Dnammentioning

confidence: 99%

“…Higher DNAm in CpG rich promoters or gene regulatory regions is usually (but not always) associated with lower gene expression [38]. While epigenetic modifications in BDNF have been frequently investigated in association with brain-related phenotypes [39], the study of their potential as biomarkers of ABI recovery is just beginning to emerge.…”

Section: Introductionmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor in Pediatric Acquired Brain Injury and Recovery

Treble-Barna,

Petersen,

Stec

et al. 2024

Biomolecules

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We review emerging preclinical and clinical evidence regarding brain-derived neurotrophic factor (BDNF) protein, genotype, and DNA methylation (DNAm) as biomarkers of outcomes in three important etiologies of pediatric acquired brain injury (ABI), traumatic brain injury, global cerebral ischemia, and stroke. We also summarize evidence suggesting that BDNF is (1) involved in the biological embedding of the psychosocial environment, (2) responsive to rehabilitative therapies, and (3) potentially modifiable. BDNF’s unique potential as a biomarker of neuroplasticity and neural repair that is reflective of and responsive to both pre- and post-injury environmental influences separates it from traditional protein biomarkers of structural brain injury with exciting potential to advance pediatric ABI management by increasing the accuracy of prognostic tools and informing clinical decision making through the monitoring of therapeutic effects.

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Brain-derived neurotrophic factor (BDNF) epigenomic modifications and brain-related phenotypes in humans: A systematic review

Cited by 13 publications

References 244 publications

Exploration of the SIRT1-mediated BDNF–TrkB signaling pathway in the mechanism of brain damage and learning and memory effects of fluorosis

Exploration of the SIRT1-mediated BDNF–TrkB signaling pathway in the mechanism of brain damage and learning and memory effects of fluorosis

Hydroxytyrosol Alleviates Obesity-Induced Cognitive Decline by Modulating the Expression Levels of Brain-Derived Neurotrophic Factors and Inflammatory Factors in Mice

Brain-Derived Neurotrophic Factor in Pediatric Acquired Brain Injury and Recovery

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