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Article ; Online: Epigenetics in fetal alcohol spectrum disorder.

Basavarajappa, Balapal S

Progress in molecular biology and translational science

2023 Volume 197, Page(s) 211–239

Abstract: During pregnancy, alcohol abuse and its detrimental effects on developing offspring are major public health, economic and social challenges. The prominent characteristic attributes of alcohol (ethanol) abuse during pregnancy in humans are neurobehavioral ...

Abstract	During pregnancy, alcohol abuse and its detrimental effects on developing offspring are major public health, economic and social challenges. The prominent characteristic attributes of alcohol (ethanol) abuse during pregnancy in humans are neurobehavioral impairments in offspring due to damage to the central nervous system (CNS), causing structural and behavioral impairments that are together named fetal alcohol spectrum disorder (FASD). Development-specific alcohol exposure paradigms were established to recapitulate the human FASD phenotypes and establish the underlying mechanisms. These animal studies have offered some critical molecular and cellular underpinnings likely to account for the neurobehavioral impairments associated with prenatal ethanol exposure. Although the pathogenesis of FASD remains unclear, emerging literature proposes that the various genomic and epigenetic components that cause the imbalance in gene expression can significantly contribute to the development of this disease. These studies acknowledged numerous immediate and enduring epigenetic modifications, such as methylation of DNA, post-translational modifications (PTMs) of histone proteins, and regulatory networks related to RNA, using many molecular approaches. Methylated DNA profiles, PTMs of histone proteins, and RNA-regulated expression of genes are essential for synaptic and cognitive behavior. Thus, offering a solution to many neuronal and behavioral impairments reported in FASD. In the current chapter, we review the recent advances in different epigenetic modifications that cause the pathogenesis of FASD. The information discussed can help better explain the pathogenesis of FASD and thereby might provide a basis for finding novel therapeutic targets and innovative treatment strategies.
MeSH term(s)	Animals ; Pregnancy ; Female ; Humans ; Fetal Alcohol Spectrum Disorders/genetics ; Histones/metabolism ; Epigenesis, Genetic ; Ethanol ; RNA ; DNA ; Prenatal Exposure Delayed Effects/genetics
Chemical Substances	Histones ; Ethanol (3K9958V90M) ; RNA (63231-63-0) ; DNA (9007-49-2)
Language	English
Publishing date	2023-02-06
Publishing country	Netherlands
Document type	Review ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2471995-X
ISSN	1878-0814 ; 0079-6603 ; 1877-1173
ISSN (online)	1878-0814
ISSN	0079-6603 ; 1877-1173
DOI	10.1016/bs.pmbts.2023.01.004
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Article ; Online: Unlocking the epigenetic symphony: histone acetylation's impact on neurobehavioral change in neurodegenerative disorders.

Basavarajappa, Balapal S / Subbanna, Shivakumar

Epigenomics

2024 Volume 16, Issue 5, Page(s) 331–358

Abstract: Recent genomics and epigenetic advances have empowered the exploration of DNA/RNA methylation and histone modifications crucial for gene expression in response to stress, aging and disease. Interest in understanding neuronal plasticity's epigenetic ... ...

Abstract	Recent genomics and epigenetic advances have empowered the exploration of DNA/RNA methylation and histone modifications crucial for gene expression in response to stress, aging and disease. Interest in understanding neuronal plasticity's epigenetic mechanisms, influencing brain rewiring amid development, aging and neurodegenerative disorders, continues to grow. Histone acetylation dysregulation, a commonality in diverse brain disorders, has become a therapeutic focus. Histone acetyltransferases and histone deacetylases have emerged as promising targets for neurodegenerative disorder treatment. This review delves into histone acetylation regulation, potential therapies and future perspectives for disorders like Alzheimer's, Parkinson's and Huntington's. Exploring genetic-environmental interplay through models and studies reveals molecular changes, behavioral insights and early intervention possibilities targeting the epigenome in at-risk individuals.
MeSH term(s)	Humans ; Histones/metabolism ; Acetylation ; Neurodegenerative Diseases/genetics ; DNA Methylation ; Epigenesis, Genetic
Chemical Substances	Histones
Language	English
Publishing date	2024-02-07
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2537199-X
ISSN	1750-192X ; 1750-1911
ISSN (online)	1750-192X
ISSN	1750-1911
DOI	10.2217/epi-2023-0428
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Article ; Online: Synaptic Plasticity Abnormalities in Fetal Alcohol Spectrum Disorders.

Basavarajappa, Balapal S / Subbanna, Shivakumar

Cells

2023 Volume 12, Issue 3

Abstract: The brain's ability to strengthen or weaken synaptic connections is often termed synaptic plasticity. It has been shown to function in brain remodeling following different types of brain damage (e.g., drugs of abuse, alcohol use disorders, ... ...

Abstract	The brain's ability to strengthen or weaken synaptic connections is often termed synaptic plasticity. It has been shown to function in brain remodeling following different types of brain damage (e.g., drugs of abuse, alcohol use disorders, neurodegenerative diseases, and inflammatory conditions). Although synaptic plasticity mechanisms have been extensively studied, how neural plasticity can influence neurobehavioral abnormalities in alcohol use disorders (AUDs) is far from being completely understood. Alcohol use during pregnancy and its harmful effects on the developing offspring are major public health, social, and economic challenges. The significant attribute of prenatal alcohol exposure on offspring is damage to the central nervous system (CNS), causing a range of synaptic structural, functional, and behavioral impairments, collectively called fetal alcohol spectrum disorder (FASD). Although the synaptic mechanisms in FASD are limited, emerging evidence suggests that FASD pathogenesis involves altering a set of molecules involved in neurotransmission, myelination, and neuroinflammation. These studies identify several immediate and long-lasting changes using many molecular approaches that are essential for synaptic plasticity and cognitive function. Therefore, they can offer potential synaptic targets for the many neurobehavioral abnormalities observed in FASD. In this review, we discuss the substantial research progress in different aspects of synaptic and molecular changes that can shed light on the mechanism of synaptic dysfunction in FASD. Increasing our understanding of the synaptic changes in FASD will significantly advance our knowledge and could provide a basis for finding novel therapeutic targets and innovative treatment strategies.
MeSH term(s)	Humans ; Female ; Pregnancy ; Fetal Alcohol Spectrum Disorders/etiology ; Fetal Alcohol Spectrum Disorders/pathology ; Alcoholism/pathology ; Prenatal Exposure Delayed Effects/pathology ; Brain/pathology ; Neuronal Plasticity
Language	English
Publishing date	2023-01-29
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12030442
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Article ; Online: Synaptic Plasticity Abnormalities in Fetal Alcohol Spectrum Disorders

Balapal S. Basavarajappa / Shivakumar Subbanna

Cells, Vol 12, Iss 442, p

2023 Volume 442

Abstract: The brain’s ability to strengthen or weaken synaptic connections is often termed synaptic ...

Abstract	The brain’s ability to strengthen or weaken synaptic connections is often termed synaptic plasticity. It has been shown to function in brain remodeling following different types of brain damage (e.g., drugs of abuse, alcohol use disorders, neurodegenerative diseases, and inflammatory conditions). Although synaptic plasticity mechanisms have been extensively studied, how neural plasticity can influence neurobehavioral abnormalities in alcohol use disorders (AUDs) is far from being completely understood. Alcohol use during pregnancy and its harmful effects on the developing offspring are major public health, social, and economic challenges. The significant attribute of prenatal alcohol exposure on offspring is damage to the central nervous system (CNS), causing a range of synaptic structural, functional, and behavioral impairments, collectively called fetal alcohol spectrum disorder (FASD). Although the synaptic mechanisms in FASD are limited, emerging evidence suggests that FASD pathogenesis involves altering a set of molecules involved in neurotransmission, myelination, and neuroinflammation. These studies identify several immediate and long-lasting changes using many molecular approaches that are essential for synaptic plasticity and cognitive function. Therefore, they can offer potential synaptic targets for the many neurobehavioral abnormalities observed in FASD. In this review, we discuss the substantial research progress in different aspects of synaptic and molecular changes that can shed light on the mechanism of synaptic dysfunction in FASD. Increasing our understanding of the synaptic changes in FASD will significantly advance our knowledge and could provide a basis for finding novel therapeutic targets and innovative treatment strategies.
Keywords	alcohol ; pregnancy ; receptors ; neurotransmitter ; gene expression ; protein expression ; Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2023-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Molecular Insights into Epigenetics and Cannabinoid Receptors.

Basavarajappa, Balapal S / Subbanna, Shivakumar

Biomolecules

2022 Volume 12, Issue 11

Abstract: The actions of cannabis are mediated by G protein-coupled receptors that are part of an endogenous cannabinoid system (ECS). ECS consists of the naturally occurring ligands N-arachidonylethanolamine (anandamide) and 2-arachidonoylglycerol (2-AG), their ... ...

Abstract	The actions of cannabis are mediated by G protein-coupled receptors that are part of an endogenous cannabinoid system (ECS). ECS consists of the naturally occurring ligands N-arachidonylethanolamine (anandamide) and 2-arachidonoylglycerol (2-AG), their biosynthetic and degradative enzymes, and the CB
MeSH term(s)	Receptors, Cannabinoid/genetics ; Proteomics ; Cannabinoids ; Cannabinoid Receptor Agonists ; Epigenesis, Genetic
Chemical Substances	Receptors, Cannabinoid ; Cannabinoids ; Cannabinoid Receptor Agonists
Language	English
Publishing date	2022-10-26
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom12111560
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Article: Endocannabinoid System and Alcohol Abuse Disorders.

Basavarajappa, Balapal S

Advances in experimental medicine and biology

2019 Volume 1162, Page(s) 89–127

Abstract: ... ...

Abstract	Δ
MeSH term(s)	Alcoholism/physiopathology ; Endocannabinoids/physiology ; Ethanol ; Humans ; Receptor, Cannabinoid, CB1/physiology ; Synapses
Chemical Substances	Endocannabinoids ; Receptor, Cannabinoid, CB1 ; Ethanol (3K9958V90M)
Language	English
Publishing date	2019-01-30
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-3-030-21737-2_6
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Article: Binge-like Prenatal Ethanol Exposure Causes Impaired Cellular Differentiation in the Embryonic Forebrain and Synaptic and Behavioral Defects in Adult Mice.

Subbanna, Shivakumar / Basavarajappa, Balapal S

Brain sciences

2022 Volume 12, Issue 6

Abstract: An embryo's in-utero exposure to ethanol due to a mother's alcohol drinking results in a range of deficits in the child that are collectively termed fetal alcohol spectrum disorders (FASDs). Prenatal ethanol exposure is one of the leading causes of ... ...

Abstract	An embryo's in-utero exposure to ethanol due to a mother's alcohol drinking results in a range of deficits in the child that are collectively termed fetal alcohol spectrum disorders (FASDs). Prenatal ethanol exposure is one of the leading causes of preventable intellectual disability. Its neurobehavioral underpinnings warrant systematic research. We investigated the immediate effects on embryos of acute prenatal ethanol exposure during gestational days (GDs) and the influence of such exposure on persistent neurobehavioral deficits in adult offspring. We administered pregnant C57BL/6J mice with ethanol (1.75 g/kg) (GDE) or saline (GDS) intraperitoneally (i.p.) at 0 h and again at 2 h intervals on GD 8 and GD 12. Subsequently, we assessed apoptosis, differentiation, and signaling events in embryo forebrains (E13.5; GD13.5). Long-lasting effects of GDE were evaluated via a behavioral test battery. We also determined the long-term potentiation and synaptic plasticity-related protein expression in adult hippocampal tissue. GDE caused apoptosis, inhibited differentiation, and reduced pERK and pCREB signaling and the expression of transcription factors Pax6 and Lhx2. GDE caused persistent spatial and social investigation memory deficits compared with saline controls, regardless of sex. Interestingly, GDE adult mice exhibited enhanced repetitive and anxiety-like behavior, irrespective of sex. GDE reduced synaptic plasticity-related protein expression and caused hippocampal synaptic plasticity (LTP and LTD) deficits in adult offspring. These findings demonstrate that binge-like ethanol exposure at the GD8 and GD12 developmental stages causes defects in pERK-pCREB signaling and reduces the expression of Pax6 and Lhx2, leading to impaired cellular differentiation during the embryonic stage. In the adult stage, binge-like ethanol exposure caused persistent synaptic and behavioral abnormalities in adult mice. Furthermore, the findings suggest that combining ethanol exposure at two sensitive stages (GD8 and GD12) causes deficits in synaptic plasticity-associated proteins (Arc, Egr1, Fgf1, GluR1, and GluN1), leading to persistent FASD-like neurobehavioral deficits in mice.
Language	English
Publishing date	2022-06-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2651993-8
ISSN	2076-3425
ISSN	2076-3425
DOI	10.3390/brainsci12060793
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Article ; Online: Histone Methylation Regulation in Neurodegenerative Disorders.

Basavarajappa, Balapal S / Subbanna, Shivakumar

International journal of molecular sciences

2021 Volume 22, Issue 9

Abstract: Advances achieved with molecular biology and genomics technologies have permitted investigators to discover epigenetic mechanisms, such as DNA methylation and histone posttranslational modifications, which are critical for gene expression in almost all ... ...

Abstract	Advances achieved with molecular biology and genomics technologies have permitted investigators to discover epigenetic mechanisms, such as DNA methylation and histone posttranslational modifications, which are critical for gene expression in almost all tissues and in brain health and disease. These advances have influenced much interest in understanding the dysregulation of epigenetic mechanisms in neurodegenerative disorders. Although these disorders diverge in their fundamental causes and pathophysiology, several involve the dysregulation of histone methylation-mediated gene expression. Interestingly, epigenetic remodeling via histone methylation in specific brain regions has been suggested to play a critical function in the neurobiology of psychiatric disorders, including that related to neurodegenerative diseases. Prominently, epigenetic dysregulation currently brings considerable interest as an essential player in neurodegenerative disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), Amyotrophic lateral sclerosis (ALS) and drugs of abuse, including alcohol abuse disorder, where it may facilitate connections between genetic and environmental risk factors or directly influence disease-specific pathological factors. We have discussed the current state of histone methylation, therapeutic strategies, and future perspectives for these disorders. While not somatically heritable, the enzymes responsible for histone methylation regulation, such as histone methyltransferases and demethylases in neurons, are dynamic and reversible. They have become promising potential therapeutic targets to treat or prevent several neurodegenerative disorders. These findings, along with clinical data, may provide links between molecular-level changes and behavioral differences and provide novel avenues through which the epigenome may be targeted early on in people at risk for neurodegenerative disorders.
MeSH term(s)	Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; Animals ; Epigenesis, Genetic ; Histone Code/genetics ; Histone Code/physiology ; Histones/genetics ; Histones/metabolism ; Humans ; Huntington Disease/genetics ; Huntington Disease/metabolism ; Methylation ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; Parkinson Disease/genetics ; Parkinson Disease/metabolism ; Protein Processing, Post-Translational ; Substance-Related Disorders/genetics ; Substance-Related Disorders/metabolism
Chemical Substances	Histones
Language	English
Publishing date	2021-04-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22094654
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Article ; Online: Histone Methylation Regulation in Neurodegenerative Disorders

Balapal S. Basavarajappa / Shivakumar Subbanna

International Journal of Molecular Sciences, Vol 22, Iss 4654, p

2021 Volume 4654

Abstract: ... such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), Amyotrophic lateral sclerosis (ALS) and ...

Abstract	Advances achieved with molecular biology and genomics technologies have permitted investigators to discover epigenetic mechanisms, such as DNA methylation and histone posttranslational modifications, which are critical for gene expression in almost all tissues and in brain health and disease. These advances have influenced much interest in understanding the dysregulation of epigenetic mechanisms in neurodegenerative disorders. Although these disorders diverge in their fundamental causes and pathophysiology, several involve the dysregulation of histone methylation-mediated gene expression. Interestingly, epigenetic remodeling via histone methylation in specific brain regions has been suggested to play a critical function in the neurobiology of psychiatric disorders, including that related to neurodegenerative diseases. Prominently, epigenetic dysregulation currently brings considerable interest as an essential player in neurodegenerative disorders, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), Amyotrophic lateral sclerosis (ALS) and drugs of abuse, including alcohol abuse disorder, where it may facilitate connections between genetic and environmental risk factors or directly influence disease-specific pathological factors. We have discussed the current state of histone methylation, therapeutic strategies, and future perspectives for these disorders. While not somatically heritable, the enzymes responsible for histone methylation regulation, such as histone methyltransferases and demethylases in neurons, are dynamic and reversible. They have become promising potential therapeutic targets to treat or prevent several neurodegenerative disorders. These findings, along with clinical data, may provide links between molecular-level changes and behavioral differences and provide novel avenues through which the epigenome may be targeted early on in people at risk for neurodegenerative disorders.
Keywords	epigenetics ; Alzheimer’s disease ; Parkinson’s disease ; Huntington’s disease ; Amyotrophic lateral sclerosis ; neuronal loss and alcohol ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2021-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Potential Mechanisms Underlying the Deleterious Effects of Synthetic Cannabinoids Found in Spice/K2 Products.

Basavarajappa, Balapal S / Subbanna, Shivakumar

Brain sciences

2019 Volume 9, Issue 1

Abstract: The chief psychoactive constituent of many bioactive phytocannabinoids (Δ⁸-tetrahydrocannabinol, Δ⁸-THC) found in hemp, cannabis or marijuana plants are scientifically denoted by the Latin term, ...

Abstract	The chief psychoactive constituent of many bioactive phytocannabinoids (Δ⁸-tetrahydrocannabinol, Δ⁸-THC) found in hemp, cannabis or marijuana plants are scientifically denoted by the Latin term,
Language	English
Publishing date	2019-01-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2651993-8
ISSN	2076-3425
ISSN	2076-3425
DOI	10.3390/brainsci9010014
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