Developmental changes in KCNQ2 and KCNQ3 expression in human brain: Possible contribution to the age-dependent etiology of benign familial neonatal convulsions

2008 ◽  
Vol 30 (5) ◽  
pp. 362-369 ◽  
Author(s):  
Takeshi Kanaumi ◽  
Sachio Takashima ◽  
Hiroshi Iwasaki ◽  
Masayuki Itoh ◽  
Akihisa Mitsudome ◽  
...  
Keyword(s):  
Human Brain ◽  
Developmental Changes ◽  
Age Dependent ◽  
Neonatal Convulsions

Age-dependent changes of glyoxalase I expression in human brain

2006 ◽  
Vol 27 (6) ◽  
pp. 815-822 ◽  
Author(s):  
Björn Kuhla ◽  
Katharina Boeck ◽  
Hans-Joachim Lüth ◽  
Angela Schmidt ◽  
Bernd Weigle ◽  
...  
Keyword(s):  
Human Brain ◽  
Glyoxalase I ◽  
Age Dependent

scholarly journals Age-dependent formation of TMEM106B amyloid filaments in human brain

2021 ◽  
Author(s):  
Manuel Schweighauser ◽  
Diana Arseni ◽  
Melissa Huang ◽  
Sofia Lövestam ◽  
Yang Shi ◽  
...  
Keyword(s):  
Human Brain ◽  
Transmembrane Protein ◽  
Amyloid Β ◽  
Dependent Manner ◽  
Type Ii ◽  
Western Blots ◽  
Normal Individuals ◽  
Age Dependent ◽  
Neurologically Normal ◽  
Filamentous Inclusions

Many age-dependent neurodegenerative diseases, like Alzheimer's and Parkinson's, are characterised by abundant inclusions of amyloid filaments. Filamentous inclusions of the proteins tau, amyloid-β (Aβ), α-synuclein and TDP-43 are the most common. Here, we used electron cryo-microscopy (cryo-EM) structure determination to show that residues 120-254 of the lysosomal type II transmembrane protein 106B (TMEM106B) also form amyloid filaments in the human brain. We solved cryo-EM structures of TMEM106B filaments from the brains of 22 individuals with neurodegenerative conditions, including sporadic and inherited tauopathies, Aβ-amyloidoses, synucleinopathies and TDP-43opathies, as well as from the brains of two neurologically normal individuals. We observed three different TMEM106B folds, with no clear relationship between folds and diseases. The presence of TMEM106B filaments correlated with that of a 29 kDa sarkosyl-insoluble fragment of the protein on Western blots. The presence of TMEM106B filaments in the brains of older, but not younger, neurologically normal individuals indicates that they form in an age-dependent manner.

Age-dependent changes in task-based modular organization of the human brain

NeuroImage ◽  
2017 ◽  
Vol 146 ◽  
pp. 741-762 ◽  
Author(s):  
Kimberly J. Schlesinger ◽  
Benjamin O. Turner ◽  
Brian A. Lopez ◽  
Michael B. Miller ◽  
Jean M. Carlson
Keyword(s):  
Human Brain ◽  
Modular Organization ◽  
Age Dependent

scholarly journals Integrated analysis of the aging brain transcriptome and proteome in tauopathy

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Carl Grant Mangleburg ◽  
Timothy Wu ◽  
Hari K. Yalamanchili ◽  
Caiwei Guo ◽  
Yi-Chen Hsieh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Human Brain ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Differentially Expressed ◽  
Integrated Analysis ◽  
Mutant Form ◽  
Brain Gene Expression ◽  
Brain Transcriptome ◽  
Age Dependent

Abstract Background Tau neurofibrillary tangle pathology characterizes Alzheimer’s disease and other neurodegenerative tauopathies. Brain gene expression profiles can reveal mechanisms; however, few studies have systematically examined both the transcriptome and proteome or differentiated Tau- versus age-dependent changes. Methods Paired, longitudinal RNA-sequencing and mass-spectrometry were performed in a Drosophila model of tauopathy, based on pan-neuronal expression of human wildtype Tau (TauWT) or a mutant form causing frontotemporal dementia (TauR406W). Tau-induced, differentially expressed transcripts and proteins were examined cross-sectionally or using linear regression and adjusting for age. Hierarchical clustering was performed to highlight network perturbations, and we examined overlaps with human brain gene expression profiles in tauopathy. Results TauWT induced 1514 and 213 differentially expressed transcripts and proteins, respectively. TauR406W had a substantially greater impact, causing changes in 5494 transcripts and 697 proteins. There was a ~ 70% overlap between age- and Tau-induced changes and our analyses reveal pervasive bi-directional interactions. Strikingly, 42% of Tau-induced transcripts were discordant in the proteome, showing opposite direction of change. Tau-responsive gene expression networks strongly implicate innate immune activation. Cross-species analyses pinpoint human brain gene perturbations specifically triggered by Tau pathology and/or aging, and further differentiate between disease amplifying and protective changes. Conclusions Our results comprise a powerful, cross-species functional genomics resource for tauopathy, revealing Tau-mediated disruption of gene expression, including dynamic, age-dependent interactions between the brain transcriptome and proteome.

Developmental changes of neuron-specific enolase in human brain: An immunohistochemical study

1985 ◽  
Vol 7 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Masaaki Nishimura ◽  
Sachio Takashima ◽  
Kenzo Takeshita ◽  
Junichi Tanaka
Keyword(s):  
Human Brain ◽  
Immunohistochemical Study ◽  
Neuron Specific Enolase ◽  
Developmental Changes

Regionally specific age-dependent decline in α2-adrenoceptors: An autoradiographic study in human brain

1991 ◽  
Vol 133 (2) ◽  
pp. 279-283 ◽  
Author(s):  
Julio Pascual ◽  
Carmen del Arco ◽  
Antonio M. González ◽  
Alvaro Díaz ◽  
Elena del Olmo ◽  
...  
Keyword(s):  
Human Brain ◽  
Autoradiographic Study ◽  
Α2 Adrenoceptors ◽  
Age Dependent

scholarly journals Age-Dependent Changes in Synaptic NMDA Receptor Composition in Adult Human Cortical Neurons

2020 ◽  
Vol 30 (7) ◽  
pp. 4246-4256 ◽  
Author(s):  
Chrysia M Pegasiou ◽  
Ardalan Zolnourian ◽  
Diego Gomez-Nicola ◽  
Katrin Deinhardt ◽  
James A R Nicoll ◽  
...  
Keyword(s):  
Human Brain ◽  
Cortical Neurons ◽  
Critical Role ◽  
Memory Storage ◽  
Neurosurgical Procedures ◽  
Adult Human ◽  
Age Related ◽  
Human Neurons ◽  
Age Dependent ◽  
Cortical Synapses

Abstract The molecular processes underlying the aging-related decline in cognitive performance and memory observed in humans are poorly understood. Studies in rodents have shown a decrease in N-methyl-D-aspartate receptors (NMDARs) that contain the GluN2B subunit in aging synapses, and this decrease is correlated with impaired memory functions. However, the age-dependent contribution of GluN2B-containing receptors to synaptic transmission in human cortical synapses has not been previously studied. We investigated the synaptic contribution of GluN2A and GluN2B-containing NMDARs in adult human neurons using fresh nonpathological temporal cortical tissue resected during neurosurgical procedures. The tissue we obtained fulfilled quality criteria by the absence of inflammation markers and proteomic degradation. We show an age-dependent decline in the NMDA/AMPA receptor ratio in adult human temporal cortical synapses. We demonstrate that GluN2B-containing NMDA receptors contribute to synaptic responses in the adult human brain with a reduced contribution in older individuals. With previous evidence demonstrating the critical role of synaptic GluN2B in regulating synaptic strength and memory storage in mice, this progressive reduction of GluN2B in the human brain during aging may underlie a molecular mechanism in the age-related decline in cognitive abilities and memory observed in humans.

Response to caffeine and ryanodine receptor isoforms in mouse skeletal muscles

2001 ◽  
Vol 281 (2) ◽  
pp. C585-C594 ◽  
Author(s):  
R. Rossi ◽  
R. Bottinelli ◽  
V. Sorrentino ◽  
C. Reggiani
Keyword(s):  
Ryanodine Receptor ◽  
Skeletal Muscles ◽  
Calcium Release ◽  
Contractile Response ◽  
Developmental Changes ◽  
Wild Type ◽  
Adult Mice ◽  
Receptor Isoforms ◽  
Age Dependent ◽  
Permeabilized Muscle

The response to caffeine was studied in mouse muscles [diaphragm, soleus, and extensor digitorum longus (EDL)] with different ryanodine receptor isoform (RyR1, RyR3) composition and in single permeabilized muscle fibers dissected from diaphragm of wild-type (WT) and RyR3-deficient (RyR3−/−) mice at 1, 15, 30, and 60 postnatal days (PND). The caffeine response decreased during development, and, in adult mice, was greater in diaphragm, lower in EDL, and intermediate in soleus. This suggests a direct relation between response to caffeine and RyR3 expression. The lack of RyR3 reduced caffeine response in young, but not in adult mice, and did not abolish the age-dependent variation and the intermuscle differences. In diaphragm single fibers, the response to caffeine increased during development and was reduced in fibers lacking RyR3 both at 15 and 60 PND. A population of fibers highly responsive to caffeine was present in adult WT and disappeared in RyR3−/−. The results confirm the contribution of RyR3 to calcium release for contractile response and clarify the contribution of RyR3 to developmental changes and intermuscle differences.

Sign in / Sign up

Export Citation Format

Share Document