TY  - JOUR
A1  - Reimann, Hauke
A1  - Stopper, Helga
A1  - Polak, Thomas
A1  - Lauer, Martin
A1  - Herrmann, Martin J.
A1  - Deckert, Jürgen
A1  - Hintzsche, Henning
T1  - Micronucleus frequency in buccal mucosa cells of patients with neurodegenerative diseases
JF  - Scientific Reports
N2  - Neurodegenerative diseases show an increase in prevalence and incidence, with the most prominent example being Alzheimer's disease. DNA damage has been suggested to play a role in the pathogenesis, but the exact mechanisms remain elusive. We enrolled 425 participants with and without neurodegenerative diseases and analyzed DNA damage in the form of micronuclei in buccal mucosa samples. In addition, other parameters such as binucleated cells, karyolytic cells, and karyorrhectic cells were quantified. No relevant differences in DNA damage and cytotoxicity markers were observed in patients compared to healthy participants. Furthermore, other parameters such as lifestyle factors and diseases were also investigated. Overall, this study could not identify a direct link between changes in buccal cells and neurogenerative diseases, but highlights the influence of lifestyle factors and diseases on the human buccal cytome.
KW  - peripheral-blood lymphocytes
KW  - Alzheimers disease
KW  - DNA damage
KW  - cognitive impairment
KW  - cytome biomarkers
KW  - diagnosis
KW  - association
KW  - assay
KW  - life
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-231430
VL  - 10
ER  - 
TY  - JOUR
A1  - Erhardt, Angelika
A1  - Meier, Sandra
A1  - Deckert, Jürgen
T1  - Genetik und Epigenetik von Angsterkrankungen
JF  - BIOspektrum
N2  - Anxiety disorders are the most common mental disorders. The etiology is complex involving genetic and environmental factors. The first genome-wide association studies so far implicate a number of genetic loci, genome-wide epigenetic and therapy response related genetic studies are emerging. Genetic studies of anxiety disorders — as the most recent Psychiatric Genomics Consortium (PGC) group of disorders — are at the threshold of providing findings comparable to other mental disorders.
KW  - Genetik
KW  - Epigenetik
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-232380
SN  - 0947-0867
VL  - 26
ER  - 
TY  - JOUR
A1  - Schaefer, Natascha
A1  - Signoret-Genest, Jérémy
A1  - von Collenberg, Cora R.
A1  - Wachter, Britta
A1  - Deckert, Jürgen
A1  - Tovote, Philip
A1  - Blum, Robert
A1  - Villmann, Carmen
T1  - Anxiety and Startle Phenotypes in Glrb Spastic and Glra1 Spasmodic Mouse Mutants
JF  - Frontiers in Molecular Neuroscience
N2  - A GWAS study recently demonstrated single nucleotide polymorphisms (SNPs) in the human GLRB gene of individuals with a prevalence for agoraphobia. GLRB encodes the glycine receptor (GlyRs) β subunit. The identified SNPs are localized within the gene flanking regions (3′ and 5′ UTRs) and intronic regions. It was suggested that these nucleotide polymorphisms modify GlyRs expression and phenotypic behavior in humans contributing to an anxiety phenotype as a mild form of hyperekplexia. Hyperekplexia is a human neuromotor disorder with massive startle phenotypes due to mutations in genes encoding GlyRs subunits. GLRA1 mutations have been more commonly observed than GLRB mutations. If an anxiety phenotype contributes to the hyperekplexia disease pattern has not been investigated yet. Here, we compared two mouse models harboring either a mutation in the murine Glra1 or Glrb gene with regard to anxiety and startle phenotypes. Homozygous spasmodic animals carrying a Glra1 point mutation (alanine 52 to serine) displayed abnormally enhanced startle responses. Moreover, spasmodic mice exhibited significant changes in fear-related behaviors (freezing, rearing and time spent on back) analyzed during the startle paradigm, even in a neutral context. Spastic mice exhibit reduced expression levels of the full-length GlyRs β subunit due to aberrant splicing of the Glrb gene. Heterozygous animals appear normal without an obvious behavioral phenotype and thus might reflect the human situation analyzed in the GWAS study on agoraphobia and startle. In contrast to spasmodic mice, heterozygous spastic animals revealed no startle phenotype in a neutral as well as a conditioning context. Other mechanisms such as a modulatory function of the GlyRs β subunit within glycinergic circuits in neuronal networks important for fear and fear-related behavior may exist. Possibly, in human additional changes in fear and fear-related circuits either due to gene-gene interactions e.g., with GLRA1 genes or epigenetic factors are necessary to create the agoraphobia and in particular the startle phenotype.
KW  - glycine receptor
KW  - spastic
KW  - fear
KW  - anxiety
KW  - startle reaction
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-210041
SN  - 1662-5099
VL  - 13
IS  - 152
ER  - 
TY  - JOUR
A1  - Deckert, Jürgen
A1  - Ozawa, Hiroki
T1  - The joint Nagasaki–Würzburg approach to challenges and perspectives in neuropsychiatric and regenerative research
JF  - Journal of Neural Transmission
N2  - No abstract available.
KW  - neuropsychiatry
KW  - regenerative research
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-235359
SN  - 0300-9564
VL  - 127
ER  -