scholarly journals 5-HT7R/G12 Signaling Regulates Neuronal Morphology and Function in an Age-Dependent Manner

2012 ◽  
Vol 32 (9) ◽  
pp. 2915-2930 ◽  
Author(s):  
F. Kobe ◽  
D. Guseva ◽  
T. P. Jensen ◽  
A. Wirth ◽  
U. Renner ◽  
...  
Keyword(s):  
Neuronal Morphology ◽  
Dependent Manner ◽  
Age Dependent ◽  
And Function

scholarly journals Age-Dependent Changes in Regulatory T Lymphocyte Development and Function: A Mini-Review

Gerontology ◽  
2017 ◽  
Vol 64 (1) ◽  
pp. 28-35 ◽  
Author(s):  
Julie Darrigues ◽  
Joost P.M. van Meerwijk ◽  
Paola Romagnoli
Keyword(s):  
T Lymphocyte ◽  
Tissue Repair ◽  
Dependent Manner ◽  
Peripheral Tissues ◽  
Regulatory T Lymphocytes ◽  
Age Dependent ◽  
And Function ◽  
Secondary Lymphoid Organs ◽  
Two Populations ◽  
Regulatory T Lymphocyte

The generation and function of immuno-suppressive regulatory T lymphocytes (Treg), which can differentiate in the thymus (tTreg) or in the periphery (pTreg), are regulated in an age-dependent manner. tTreg are produced at high levels in the first weeks of age, when they expand and colonize secondary lymphoid organs and peripheral tissues to protect the organism from autoimmune diseases and to promote tissue repair. Once this population of Treg is operational in the periphery, at puberty, thymic output of Treg declines, but self-reactive tTreg generated early on in life are maintained over time and play a major role in preserving homeostasis of the immune system. Extra-thymic pTreg differentiation declines later on in life. pTreg generated throughout life mainly protect the organism from chronic inflammation and the semi-allogeneic fetus from rejection. In this review, age-dependent modulation of the production and function of these two populations of Treg is described.

scholarly journals A LRRK2/dLRRK-mediated lysosomal pathway that contributes to glial cell death and DA neuron survival

2021 ◽  
Author(s):  
Linfang Wang ◽  
Honglei Wang ◽  
Margaret S Ho
Keyword(s):  
Caspase 3 ◽  
Kinase Activity ◽  
Dependent Manner ◽  
Dopaminergic Neurodegeneration ◽  
Age Dependent ◽  
Sporadic Parkinson’S Disease ◽  
Locomotor Deficits ◽  
And Function ◽  
Reduced Activity

Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common cause of familial and sporadic Parkinson's disease (PD). A plethora of evidence has indicated a role for LRRK2 in endolysosomal trafficking in neurons, while LRRK2 function in glia, although highly expressed, remains largely unknown. Here we present evidence that LRRK2/dLRRK mediates a glial lysosomal pathway that contributes to the mechanism of PD. Independent of its kinase activity, glial LRRK2/dLRRK knockdown in the immortalized microglial cells or flies results in enlarged and swelling lysosomes fewer in number. These lysosomes are less mobile, wrongly acidified, and exhibit defective membrane permeability and reduced activity of the lysosome hydrolase cathespin B. In addition, microglial LRRK2 depletion causes increased Caspase 3 levels, leading to glial apoptosis, dopaminergic neurodegeneration, and locomotor deficits in an age-dependent manner. Taken together, these findings demonstrate a functional role of LRRK2/dLRRK in regulating the glial lysosomal pathway; deficits in lysosomal biogenesis and function linking to glial apoptosis potentially underlie the mechanism of DA neurodegeneration, contributing to the progression of PD.

scholarly journals Age-dependent dormant resident progenitors are stimulated by injury to regenerate Purkinje neurons

2018 ◽  
Author(s):  
N. Sumru Bayin ◽  
Alexandre Wojcinski ◽  
Aurelien Mourton ◽  
Hiromitsu Saito ◽  
Noboru Suzuki ◽  
...  
Keyword(s):  
Dependent Manner ◽  
New Paradigm ◽  
Perinatal Brain Injury ◽  
Cerebellar Function ◽  
Efficient Regeneration ◽  
Age Dependent ◽  
Cerebellum Development ◽  
And Function ◽  
The Brain ◽  
Normal Cerebellum

AbstractOutside of the neurogenic niches of the brain, postmitotic neurons have not been found to undergo efficient regeneration. Here we demonstrate that Purkinje cells (PCs), which are born at midgestation and are crucial for both development and function of cerebellar circuits, are rapidly and fully regenerated following their ablation at birth. New PCs are produced by a previously unidentified progenitor population and support normal cerebellum development. The number of PC progenitors and their regenerative capacity, however, diminish soon after birth, and consequently PCs are poorly replenished when ablated at postnatal day 5. Nevertheless, the PC-depleted cerebella reach a normal size by increasing cell size, but scaling of neuron types is disrupted and cerebellar function is impaired. Our findings thus provide a new paradigm in the field of neuron regeneration by identifying a unipotent neural progenitor that buffers against perinatal brain injury in a stage-dependent process.One sentence summaryInjury induces a dormant progenitor population present at birth to regenerate cerebellar neurons in a time-dependent manner.

Second-trimester maternal lipid profiles predict pregnancy complications in an age-dependent manner

2019 ◽  
Vol 299 (5) ◽  
pp. 1253-1260 ◽  
Author(s):  
Qi Wu ◽  
Lixia Zhang ◽  
Licong Huang ◽  
Yu Lei ◽  
Lin Chen ◽  
...  
Keyword(s):  
Pregnancy Complications ◽  
Lipid Profiles ◽  
Dependent Manner ◽  
Second Trimester ◽  
Age Dependent

Deletion of murine tau gene increases tau aggregation in a human mutant tau transgenic mouse model

2010 ◽  
Vol 38 (4) ◽  
pp. 1001-1005 ◽  
Author(s):  
Kunie Ando ◽  
Karelle Leroy ◽  
Céline Heraud ◽  
Anna Kabova ◽  
Zehra Yilmaz ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mouse ◽  
Double Mutant ◽  
Transgenic Mouse Model ◽  
Tau Proteins ◽  
Dependent Manner ◽  
Age Dependent ◽  
Ad Alzheimer’S Disease ◽  
Tau Aggregation ◽  
The Brain

We have reported previously a tau transgenic mouse model (Tg30tau) overexpressing human 4R1N double-mutant tau (P301S and G272V) and that develops AD (Alzheimer's disease)-like NFTs (neurofibrillary tangles) in an age-dependent manner. Since murine tau might interfere with the toxic effects of human mutant tau, we set out to analyse the phenotype of our Tg30tau model in the absence of endogenous murine tau with the aim to reproduce more faithfully a model of human tauopathy. By crossing the Tg30tau line with TauKO (tau-knockout) mice, we have obtained a new mouse line called Tg30×TauKO that expresses only exogenous human double-mutant 4R1N tau. Whereas Tg30×TauKO mice express fewer tau proteins compared with Tg30tau, they exhibit augmented sarkosyl-insoluble tau in the brain and an increased number of Gallyas-positive NFTs in the hippocampus. Taken together, exclusion of murine tau causes accelerated tau aggregation during aging of this mutant tau transgenic model.

scholarly journals Random errors in protein synthesis activate an age-dependent program of muscle atrophy in mice

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
James Moore ◽  
Rashid Akbergenov ◽  
Martina Nigri ◽  
Patricia Isnard-Petit ◽  
Amandine Grimm ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Muscle Atrophy ◽  
Strength Analysis ◽  
Dependent Manner ◽  
Random Errors ◽  
Age Related ◽  
Related Phenotype ◽  
Age Dependent ◽  
Translation Accuracy ◽  
Transcriptomic Changes

AbstractRandom errors in protein synthesis are prevalent and ubiquitous, yet their effect on organismal health has remained enigmatic for over five decades. Here, we studied whether mice carrying the ribosomal ambiguity (ram) mutation Rps2-A226Y, recently shown to increase the inborn error rate of mammalian translation, if at all viable, present any specific, possibly aging-related, phenotype. We introduced Rps2-A226Y using a Cre/loxP strategy. Resulting transgenic mice were mosaic and showed a muscle-related phenotype with reduced grip strength. Analysis of gene expression in skeletal muscle using RNA-Seq revealed transcriptomic changes occurring in an age-dependent manner, involving an interplay of PGC1α, FOXO3, mTOR, and glucocorticoids as key signaling pathways, and finally resulting in activation of a muscle atrophy program. Our results highlight the relevance of translation accuracy, and show how disturbances thereof may contribute to age-related pathologies.

TRPV1 deletion exacerbates hyperthermic seizures in an age-dependent manner in mice

2016 ◽  
Vol 128 ◽  
pp. 27-34 ◽  
Author(s):  
Karlene T. Barrett ◽  
Richard J.A. Wilson ◽  
Morris H. Scantlebury
Keyword(s):  
Dependent Manner ◽  
Age Dependent

scholarly journals WD40-repeat 47, a microtubule-associated protein, is essential for brain development and autophagy

2017 ◽  
Vol 114 (44) ◽  
pp. E9308-E9317 ◽  
Author(s):  
Meghna Kannan ◽  
Efil Bayam ◽  
Christel Wagner ◽  
Bruno Rinaldi ◽  
Perrine F. Kretz ◽  
...  
Keyword(s):  
Corpus Callosum ◽  
Brain Development ◽  
Brain Connectivity ◽  
Neuronal Morphology ◽  
Dependent Manner ◽  
Wd40 Repeat ◽  
Starting Point ◽  
Neuronal Regulation ◽  
The Family ◽  
Cervical Ganglion

The family of WD40-repeat (WDR) proteins is one of the largest in eukaryotes, but little is known about their function in brain development. Among 26 WDR genes assessed, we found 7 displaying a major impact in neuronal morphology when inactivated in mice. Remarkably, all seven genes showed corpus callosum defects, including thicker (Atg16l1, Coro1c, Dmxl2, and Herc1), thinner (Kif21b and Wdr89), or absent corpus callosum (Wdr47), revealing a common role for WDR genes in brain connectivity. We focused on the poorly studied WDR47 protein sharing structural homology with LIS1, which causes lissencephaly. In a dosage-dependent manner, mice lacking Wdr47 showed lethality, extensive fiber defects, microcephaly, thinner cortices, and sensory motor gating abnormalities. We showed that WDR47 shares functional characteristics with LIS1 and participates in key microtubule-mediated processes, including neural stem cell proliferation, radial migration, and growth cone dynamics. In absence of WDR47, the exhaustion of late cortical progenitors and the consequent decrease of neurogenesis together with the impaired survival of late-born neurons are likely yielding to the worsening of the microcephaly phenotype postnatally. Interestingly, the WDR47-specific C-terminal to LisH (CTLH) domain was associated with functions in autophagy described in mammals. Silencing WDR47 in hypothalamic GT1-7 neuronal cells and yeast models independently recapitulated these findings, showing conserved mechanisms. Finally, our data identified superior cervical ganglion-10 (SCG10) as an interacting partner of WDR47. Taken together, these results provide a starting point for studying the implications of WDR proteins in neuronal regulation of microtubules and autophagy.

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