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Article ; Online: Sex Differences in the Expression of the α5 Subunit of the GABA

Janeczek, Paulina / Colson, Natalie / Dodd, Peter R / Lewohl, Joanne M

Alcoholism, clinical and experimental research

2020 Volume 44, Issue 2, Page(s) 423–434

Abstract: Background: Alcohol exposure alters the expression of a large number of genes, resulting in neuronal adaptions and neuronal loss, but the underlying mechanisms are largely unknown. miRNAs are gene repressors that are abundant in the brain. A recent ... ...

Abstract	Background: Alcohol exposure alters the expression of a large number of genes, resulting in neuronal adaptions and neuronal loss, but the underlying mechanisms are largely unknown. miRNAs are gene repressors that are abundant in the brain. A recent study identified ~ 35 miRNAs that are up-regulated in the prefrontal cortex of human alcoholics and predicted to target genes that are down-regulated in the same region. Although interactions between alcohol-responsive miRNAs and their target genes have been predicted, few studies have validated these predictions. Methods: We measured the expression of GABA Results: In both frontal and motor cortices, the expression of GABA Conclusion: There are sex differences in the expression of GABA
MeSH term(s)	Adult ; Aged ; Alcoholics ; Alcoholism/epidemiology ; Alcoholism/genetics ; Alcoholism/metabolism ; Cohort Studies ; Female ; Gene Expression ; HEK293 Cells ; Humans ; Liver Cirrhosis, Alcoholic/epidemiology ; Liver Cirrhosis, Alcoholic/genetics ; Liver Cirrhosis, Alcoholic/metabolism ; Male ; Middle Aged ; Motor Cortex/metabolism ; Prefrontal Cortex/metabolism ; Receptors, GABA-A/biosynthesis ; Receptors, GABA-A/genetics ; Sex Characteristics
Chemical Substances	GABRA5 protein, human ; Receptors, GABA-A
Language	English
Publishing date	2020-01-09
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	428999-7
ISSN	1530-0277 ; 0145-6008
ISSN (online)	1530-0277
ISSN	0145-6008
DOI	10.1111/acer.14266
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Article ; Online: New insights into Alzheimer's disease pathogenesis: the involvement of neuroligins in synaptic malfunction.

Sindi, Ikhlas A / Dodd, Peter R

Neurodegenerative disease management

2015 Volume 5, Issue 2, Page(s) 137–145

Abstract: Synaptic damage is a key hallmark of Alzheimer's disease and the best correlate with cognitive decline ante mortem. Signature protein combinations arrayed at tightly apposed pre- and post-synaptic sites characterize different types of synapse. ... ...

Abstract	Synaptic damage is a key hallmark of Alzheimer's disease and the best correlate with cognitive decline ante mortem. Signature protein combinations arrayed at tightly apposed pre- and post-synaptic sites characterize different types of synapse. Neuroligins are postsynaptic cell adhesion molecules that interact with neurexins across the synaptic cleft. These pairings recruit receptors, channels and signal transduction molecules to the synapse, and help mediate trans-synaptic transmission. Dysfunction in the neuroligin family can disrupt neuronal networks and leads to neurodegeneration and other diseases. The extracellular domain of neuroligins is homologous with acetylcholinesterase but lacks residues required for enzymatic activity. This domain may interact pathogenically with β-amyloid. Here we summarize research over the last decade on the potential involvement of neuroligins in Alzheimer's disease.
MeSH term(s)	Alzheimer Disease/physiopathology ; Animals ; Cell Adhesion Molecules, Neuronal/metabolism ; Humans ; Synapses/physiology ; Synaptic Transmission/physiology
Chemical Substances	Cell Adhesion Molecules, Neuronal
Language	English
Publishing date	2015
Publishing country	England
Document type	Journal Article ; Review
ISSN	1758-2032
ISSN (online)	1758-2032
DOI	10.2217/nmt.14.54
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Article ; Online: Emerging roles for brain drug-metabolizing cytochrome P450 enzymes in neuropsychiatric conditions and responses to drugs.

Toselli, Francesca / Dodd, Peter R / Gillam, Elizabeth M J

Drug metabolism reviews

2016 Volume 48, Issue 3, Page(s) 379–404

Abstract: P450s in the human brain were originally considered unlikely to contribute significantly to the clearance of drugs and other xenobiotic chemicals, since their overall expression was a small fraction of that found in the liver. However, it is now ... ...

Abstract	P450s in the human brain were originally considered unlikely to contribute significantly to the clearance of drugs and other xenobiotic chemicals, since their overall expression was a small fraction of that found in the liver. However, it is now recognized that P450s play substantial roles in the metabolism of both exogenous and endogenous chemicals in the brain, but in a highly cell type- and region-specific manner, in line with the greater functional heterogeneity of the brain compared to the liver. Studies of brain P450 expression and the characterization of the catalytic activity of specific forms expressed as recombinant enzymes have suggested possible roles for xenobiotic-metabolizing P450s in the brain. It is now possible to confirm these roles through the use of intracerebroventricular administration of selective P450 inhibitors in animal models, coupled with brain sampling techniques to measure drug concentrations in vivo, and modern neuroimaging techniques. The purpose of this review is to discuss the evidence behind the functional importance of P450s from the "xenobiotic-metabolizing" families, CYP1, CYP2 and CYP3 in the brain. Approaches used to define the quantitative and qualitative significance of these P450s in determining tissue-specific levels of xenobiotics in brain will be considered. Finally, the possible roles of these enzymes in brain biochemistry will be examined in light of the demonstrated activity of these enzymes in vitro and the association of particular P450 forms with disease states.
MeSH term(s)	Animals ; Brain/enzymology ; Brain/physiology ; Cytochrome P-450 Enzyme Inhibitors/pharmacology ; Cytochrome P450 Family 1/metabolism ; Cytochrome P450 Family 1/physiology ; Cytochrome P450 Family 2/metabolism ; Cytochrome P450 Family 2/physiology ; Cytochrome P450 Family 3/metabolism ; Cytochrome P450 Family 3/physiology ; Humans ; Liver/metabolism ; Mental Disorders/enzymology ; Mental Disorders/physiopathology ; Xenobiotics/metabolism
Chemical Substances	Cytochrome P-450 Enzyme Inhibitors ; Xenobiotics ; Cytochrome P450 Family 1 (EC 1.14.14.1) ; Cytochrome P450 Family 2 (EC 1.14.14.1) ; Cytochrome P450 Family 3 (EC 1.14.14.1)
Language	English
Publishing date	2016-08
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	184967-0
ISSN	1097-9883 ; 0360-2532 ; 0012-6594
ISSN (online)	1097-9883
ISSN	0360-2532 ; 0012-6594
DOI	10.1080/03602532.2016.1221960
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Article ; Online: Nucleic Acid-Based Theranostics for Tackling Alzheimer's Disease.

Chakravarthy, Madhuri / Chen, Suxiang / Dodd, Peter R / Veedu, Rakesh N

Theranostics

2017 Volume 7, Issue 16, Page(s) 3933–3947

Abstract: Nucleic acid-based technologies have received significant interest in recent years as novel theranostic strategies for various diseases. The approval by the United States Food and Drug Administration (FDA) of Nusinersen, an antisense oligonucleotide drug, ...

Abstract	Nucleic acid-based technologies have received significant interest in recent years as novel theranostic strategies for various diseases. The approval by the United States Food and Drug Administration (FDA) of Nusinersen, an antisense oligonucleotide drug, for the treatment of spinal muscular dystrophy highlights the potential of nucleic acids to treat neurological diseases, including Alzheimer's disease (AD). AD is a devastating neurodegenerative disease characterized by progressive impairment of cognitive function and behavior. It is the most common form of dementia; it affects more than 20% of people over 65 years of age and leads to death 7-15 years after diagnosis. Intervention with novel agents addressing the underlying molecular causes is critical. Here we provide a comprehensive review on recent developments in nucleic acid-based theranostic strategies to diagnose and treat AD.
MeSH term(s)	Alzheimer Disease/diagnosis ; Amyloid beta-Peptides/metabolism ; Animals ; Clinical Trials as Topic ; Humans ; Nucleic Acids/therapeutic use ; Theranostic Nanomedicine ; tau Proteins/metabolism
Chemical Substances	Amyloid beta-Peptides ; Nucleic Acids ; tau Proteins
Language	English
Publishing date	2017-09-05
Publishing country	Australia
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.21529
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Article: Multiple reaction monitoring for the detection of disease-related synaptic proteins.

Chang, Rachel Yoon Kyung / Dodd, Peter R

Neural regeneration research

2015 Volume 9, Issue 23, Page(s) 2042–2043

Language	English
Publishing date	2015-01-22
Publishing country	India
Document type	Journal Article
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.147926
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Article ; Online: Sex differences in GABA

Ashton, Madeline K / Rueda, André V L / Ho, Ada M-C / Noor Aizin, Noradibah Arina Binte M / Sharma, Hansa / Dodd, Peter R / Stadlin, Alfreda / Camarini, Rosana

Genes, brain, and behavior

2022 Volume 21, Issue 4, Page(s) e12785

Abstract: Male and female human subjects show contrasting propensities to misuse drugs of addiction, including alcohol. These differences lead to different psychological and neurological consequences, such as the likelihood of developing dependence. The pattern ... ...

Abstract	Male and female human subjects show contrasting propensities to misuse drugs of addiction, including alcohol. These differences lead to different psychological and neurological consequences, such as the likelihood of developing dependence. The pattern and extent of brain damage in alcohol-use disorder cases also varies with comorbid disease. To explore mechanisms that might underlie these outcomes, we used autopsy tissue to determine mRNA transcript expression in relation to genotype for two GABA
MeSH term(s)	Alcoholism/genetics ; Alcoholism/metabolism ; Female ; Genotype ; Humans ; Liver Cirrhosis/genetics ; Male ; Polymorphism, Single Nucleotide ; Receptors, GABA-A/genetics ; Sex Characteristics
Chemical Substances	Receptors, GABA-A
Language	English
Publishing date	2022-03-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2075819-4
ISSN	1601-183X ; 1601-1848
ISSN (online)	1601-183X
ISSN	1601-1848
DOI	10.1111/gbb.12785
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Zs.A 5642: Show issues

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Article ; Online: Electrically evoked synaptosomal amino acid transmitter release in human brain in alcohol misuse.

Kuo, Sheng-Wen / Dodd, Peter R

Neuro-Signals

2011 Volume 19, Issue 3, Page(s) 117–127

Abstract: Severe chronic alcohol misuse leads to neuropathological changes in human brain, with the greatest neuronal loss in the dorsolateral prefrontal cortex. In this region, GABA(A) receptors are selectively upregulated, and show altered subunit expression ... ...

Abstract	Severe chronic alcohol misuse leads to neuropathological changes in human brain, with the greatest neuronal loss in the dorsolateral prefrontal cortex. In this region, GABA(A) receptors are selectively upregulated, and show altered subunit expression profiles only in alcoholics without comorbid disease, whereas glutamate(NMDA) subunit expression profiles are selectively downregulated only in alcoholics with comorbid cirrhosis of the liver. To determine whether these outcomes might be conditional on synaptic transmitter levels, evoked release was studied in well-characterized synaptosome suspensions preloaded with L-[(3)H]glutamate and [(14)C]GABA and stimulated electrically (±10 V contiguous square waves, 0.4 ms, 100 Hz, 1.5 min) with and without Ca(2+). Stimulation elicited brief peaks of both radioisotopes that were larger in the presence of Ca(2+) ions (p < 0.01). A repeat stimulus evoked a second, smaller (p < 0.01) peak. Ca(2+)-dependent L-[(3)H]glutamate release, but not [(14)C]GABA release, was higher overall in alcoholics than in controls (p < 0.05). With comorbid cirrhosis, L-[(3)H]glutamate release showed a graded response, whereas [(14)C]GABA release was lowest in noncirrhotic alcoholics. Release patterns did not differ between cortical regions, or between males and females. Neither age nor postmortem interval was a significant confounder. The released transmitters may differentially alter receptor profiles on postsynaptic cells.
MeSH term(s)	Adult ; Age Factors ; Aged ; Aged, 80 and over ; Alcoholism/pathology ; Amino Acids/metabolism ; Analysis of Variance ; Area Under Curve ; Biophysics ; Brain/pathology ; Brain/ultrastructure ; Calcium/pharmacology ; Carbon Isotopes/metabolism ; Electric Stimulation/methods ; Female ; Humans ; In Vitro Techniques ; Isotopes/metabolism ; Liver Cirrhosis, Alcoholic/pathology ; Male ; Middle Aged ; Sex Factors ; Synaptosomes/drug effects ; Synaptosomes/metabolism ; Synaptosomes/radiation effects ; Time Factors ; Young Adult
Chemical Substances	Amino Acids ; Carbon Isotopes ; Isotopes ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2011-08-11
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2074039-6
ISSN	1424-8638 ; 1424-862X
ISSN (online)	1424-8638
ISSN	1424-862X
DOI	10.1159/000326842
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Article ; Online: Role for the neurexin-neuroligin complex in Alzheimer's disease.

Sindi, Ikhlas A / Tannenberg, Rudolph K / Dodd, Peter R

Neurobiology of aging

2014 Volume 35, Issue 4, Page(s) 746–756

Abstract: Synaptic damage is a critical hallmark of Alzheimer's disease, and the best correlate with cognitive impairment ante mortem. Synapses, the loci of communication between neurons, are characterized by signature protein combinations arrayed at tightly ... ...

Abstract	Synaptic damage is a critical hallmark of Alzheimer's disease, and the best correlate with cognitive impairment ante mortem. Synapses, the loci of communication between neurons, are characterized by signature protein combinations arrayed at tightly apposed pre- and post-synaptic sites. The most widely studied trans-synaptic junctional complexes, which direct synaptogenesis and foster the maintenance and stability of the mature terminal, are conjunctions of presynaptic neurexins and postsynaptic neuroligins. Fluctuations in the levels of neuroligins and neurexins can sway the balance between excitatory and inhibitory neurotransmission in the brain, and could lead to damage of synapses and dendrites. This review summarizes current understanding of the roles of neurexins and neuroligins proteolytic processing in synaptic plasticity in the human brain, and outlines their possible roles in β-amyloid metabolism and function, which are central pathogenic events in Alzheimer's disease progression.
MeSH term(s)	Acetylcholinesterase/physiology ; Alternative Splicing/physiology ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Alzheimer Disease/psychology ; Amyloid beta-Peptides/metabolism ; Brain/metabolism ; Brain/pathology ; Brain/physiopathology ; Cell Adhesion Molecules, Neuronal ; Cell Communication/genetics ; Cell Communication/physiology ; Disease Progression ; Humans ; Learning ; Memory ; Nerve Tissue Proteins ; Neural Cell Adhesion Molecules/physiology ; Neuronal Plasticity/genetics ; Neuronal Plasticity/physiology ; Neurons/pathology ; Neurons/physiology ; Synapses/genetics ; Synapses/pathology ; Synapses/physiology
Chemical Substances	Amyloid beta-Peptides ; Cell Adhesion Molecules, Neuronal ; NRXN1 protein, human ; Nerve Tissue Proteins ; Neural Cell Adhesion Molecules ; neuroligin 1 ; Acetylcholinesterase (EC 3.1.1.7)
Language	English
Publishing date	2014-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2013.09.032
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Article: Excited to death: different ways to lose your neurones.

Dodd, Peter R

Biogerontology

2002 Volume 3, Issue 1-2, Page(s) 51–56

Abstract: The selective loss of neurones in a range of neurodegenerative diseases is widely thought to involve the process of excitotoxicity, in which glutamate-mediated neuronal killing is elaborated through the excessive stimulation of cell-surface receptors. ... ...

Abstract	The selective loss of neurones in a range of neurodegenerative diseases is widely thought to involve the process of excitotoxicity, in which glutamate-mediated neuronal killing is elaborated through the excessive stimulation of cell-surface receptors. Every such disease exhibits a distinct regional and subregional pattern of neuronal loss, so processes must be locally triggered to different extents to account for this. We have studied several mechanisms which could lead to excitotoxic glutamate pathophysiology and compared them in different diseases. Our data suggest that glutamate can reach toxic extracellular levels in Alzheimer disease by malfunctions in cellular transporters, and that the toxicity may be exacerbated by continued glutamate release from presynaptic neurones acting on hypersensitive postsynaptic receptors. Thus the excitotoxicity is direct. In contrast, alcoholic brain damage arises in regions where GABA-mediated inhibition is deficient, and fails properly to dampen trans-synaptic excitation. Thus the excitotoxicity is indirect. A variety of such mechanisms is possible, which may combine in different ways.
MeSH term(s)	Animals ; Cell Death ; Excitatory Amino Acids/physiology ; Humans ; Neurons/pathology
Chemical Substances	Excitatory Amino Acids
Language	English
Publishing date	2002-05-13
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2047160-9
ISSN	1389-5729
ISSN	1389-5729
DOI	10.1023/a:1015255312948
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Zs.A 5706: Show issues

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Article ; Online: SWATH analysis of the synaptic proteome in Alzheimer's disease.

Chang, Rachel Yoon Kyung / Etheridge, Naomi / Nouwens, Amanda S / Dodd, Peter R

Neurochemistry international

2015 Volume 87, Page(s) 1–12

Abstract: Brain tissue from Alzheimer's disease patients exhibits synaptic degeneration in selected regions. Synaptic dysfunction occurs early in the disease and is a primary pathological target for treatment. The molecular mechanisms underlying this degeneration ... ...

Abstract	Brain tissue from Alzheimer's disease patients exhibits synaptic degeneration in selected regions. Synaptic dysfunction occurs early in the disease and is a primary pathological target for treatment. The molecular mechanisms underlying this degeneration remain unknown. Quantifying the synaptic proteome in autopsy brain and comparing tissue from Alzheimer's disease cases and subjects with normal aging are critical to understanding the molecular mechanisms associated with Alzheimer pathology. We isolated synaptosomes from hippocampus and motor cortex so as to reduce sample complexity relative to whole-tissue homogenates. Synaptosomal extracts were subjected to strong cation exchange (SCX) fractionation to further partition sample complexity; each fraction received SWATH-based information-dependent acquisition to generate a comprehensive peptide-ion library. The expression of synaptic proteins from AD hippocampus and motor cortex was then compared between groups. A total of 2077 unique proteins were identified at a critical local false discovery rate <5%. Thirty of these, including 17 novel proteins, exhibited significant expression differences between cases and controls; these proteins are involved in cellular functions including structural maintenance, signal transduction, autophagy, oxidative stress, and proteasome activity, or they have synaptic-vesicle related or energy-related functions. Differentially expressed proteins were subjected to pathway analysis to identify protein-protein interactions. This revealed that the most perturbed molecular and cellular functions were cellular assembly and organization. Core analysis revealed RhoA signaling to be the top canonical pathway. Network analysis showed that differentially expressed proteins were related to cellular assembly and organization, and cellular function and maintenance. This is the first study to combine SCX fractionation with SWATH analysis. SWATH is a promising new technique that can greatly enhance protein identification in any proteome, and has many other benefits; however, there are limitations yet to be resolved.
MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/metabolism ; Female ; Humans ; Male ; Nerve Tissue Proteins/metabolism ; Proteome ; Synapses/metabolism
Chemical Substances	Nerve Tissue Proteins ; Proteome
Language	English
Publishing date	2015-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	283190-9
ISSN	1872-9754 ; 0197-0186
ISSN (online)	1872-9754
ISSN	0197-0186
DOI	10.1016/j.neuint.2015.04.004
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