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Natural killer cells in aging and age-related diseases
Neurobiol Dis. 2023 May 18:106156. doi: 10.1016/j.nbd.2023.106156. Online ahead of print.ABSTRACTAging leads to escalated systemic inflammation. As the sentinel of immune system, natural killer (NK) cells are early responders that sense cues and signals from target organs and swiftly orchestrate local inflammation upon their arrival. Emerging evidence indicates a profound role of NK cells in the initiation and evolution of neuroinflammation in aging and age-related diseases. Here we discuss recent advances in NK cell biology and the organ-specific features of NK cells in normal brain aging, Alzheimer's disease, Parkinson's...
Source: Neurobiology of Disease - May 20, 2023 Category: Neurology Authors: Caiyun Qi Qiang Liu Source Type: research

Primary cilia and ciliary signaling pathways in aging and age-related brain disorders
Neurobiol Dis. 2022 Feb;163:105607. doi: 10.1016/j.nbd.2021.105607. Epub 2021 Dec 31.ABSTRACTBrain disorders are characterized by the progressive loss of structure and function of the brain as a consequence of progressive degeneration and/or death of nerve cells. Aging is a major risk factor for brain disorders such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and stroke. Various cellular and molecular events have been shown to play a role in the progress of neurodegenerative diseases. Emerging studies suggest that primary cilia could be a key regulator in brain diseases. The ...
Source: Neurobiology of Disease - January 3, 2022 Category: Neurology Authors: Rong Ma Naseer A Kutchy Liang Chen Douglas D Meigs Guoku Hu Source Type: research

T1AM-TAAR1 signalling protects against OGD-induced synaptic dysfunction in the entorhinal cortex.
Abstract Abnormalities in thyroid hormones (TH) availability and/or metabolism have been hypothesized to contribute to Alzheimer's disease (AD) and to be a risk factor for stroke. Recently, 3-iodothyronamine (T1AM), an endogenous amine putatively derived from TH metabolism, gained interest for its ability to promote learning and memory in the mouse. Moreover, T1AM has been demonstrated to rescue the β-Amyloid dependent LTP impairment in the entorhinal cortex (EC), a brain area crucially involved in learning and memory and early affected during AD. In the present work, we have investigated the effect of T1AM on is...
Source: Neurobiology of Disease - January 19, 2021 Category: Neurology Authors: Tozzi F, Rutigliano G, Borsò M, Falcicchia C, Zucchi R, Origlia N Tags: Neurobiol Dis Source Type: research

Epigenetic regulators of neuronal ferroptosis identify novel therapeutics for neurological diseases: HDACs, transglutaminases, and HIF prolyl hydroxylases.
Abstract A major thrust of our laboratory has been to identify how physiological stress is transduced into transcriptional responses that feed back to overcome the inciting stress or its consequences, thereby fostering survival and repair. To this end, we have adopted the use of an in vitro model of ferroptosis, a caspase-independent, but iron-dependent form of cell death (Dixon et al., 2012; Ratan, 2020). In this review, we highlight three distinct epigenetic targets that have evolved from our studies and which have been validated in vivo studies. In the first section, we discuss our studies of broad, pan-selecti...
Source: Neurobiology of Disease - October 27, 2020 Category: Neurology Authors: Rroji O, Kumar A, Karuppagounder SS, Ratan RR Tags: Neurobiol Dis Source Type: research

Immunotherapy for Parkinson's disease.
Abstract With the increasing prevalence of Parkinson's disease, there is an immediate need to interdict disease signs and symptoms. In recent years this need was met through therapeutic approaches focused on regenerative stem cell replacement and alpha-synuclein clearance. However, neither have shown long-term clinical benefit. A novel therapeutic approach designed to affect disease is focused on transforming the brain's immune microenvironment. As disordered innate and adaptive immune functions are primary components of neurodegenerative disease pathogenesis, this has emerged as a clear opportunity for therapeuti...
Source: Neurobiology of Disease - January 20, 2020 Category: Neurology Authors: Schwab AD, Thurston MJ, Machhi JP, Olson KE, Namminga KL, Gendelman HE, Mosley RL Tags: Neurobiol Dis Source Type: research

KCa3.1 deficiency attenuates neuroinflammation by regulating an astrocyte phenotype switch involving the PI3K/AKT/GSK3 β pathway.
KCa3.1 deficiency attenuates neuroinflammation by regulating an astrocyte phenotype switch involving the PI3K/AKT/GSK3β pathway. Neurobiol Dis. 2019 Aug 27;:104588 Authors: Wei T, Wang Y, Xu W, Yan L, Chen H, Yu Z Abstract Neuroinflammation may induce a phenotype switch to reactive astrogliosis in neurodegenerative disorders. The calcium-activated potassium channel (KCa3.1) is active in the phenotypic switch that occurs during astrogliosis in Alzheimer's disease and ischemic stroke. Here, transcriptome sequencing (RNA-Seq), immunohistochemistry, western blotting, pharmacological blockade, and calcium...
Source: Neurobiology of Disease - August 26, 2019 Category: Neurology Authors: Wei T, Wang Y, Xu W, Yan L, Chen H, Yu Z Tags: Neurobiol Dis Source Type: research

Decline in Sirtuin-1 expression and activity plays a critical role in blood-brain barrier permeability in aging.
Abstract Accumulating evidence suggest that cerebral microvascular disease increases with advancing age and is associated with lacunar stroke, leukoaraiosis, vascular dementia and Alzheimer disease. Increased blood brain barrier (BBB) permeability/leakage takes "center stage" in ongoing age-related vascular/brain parenchymal injury. Although significant effort has been made in defining the gene mutations and risk factors involved in microvascular alterations in vascular dementia and Alzheimer disease, the intra- and intercellular pathogenic mechanisms responsible for vascular hyperpermeability are still largely un...
Source: Neurobiology of Disease - September 6, 2018 Category: Neurology Authors: Stamatovic SM, Martinez GR, Hu A, Choi J, Keep RF, Andjelkovic AV Tags: Neurobiol Dis Source Type: research

Inflammation at the blood-brain barrier: The role of liver X receptors.
Abstract The blood-brain barrier (BBB) is indispensable for the maintenance of brain homeostasis and proper neuronal functioning. Dysfunction of the BBB significantly contributes to the pathogenesis of neuroinflammatory and neurodegenerative diseases like stroke, multiple sclerosis (MS), and Alzheimer's disease (AD). The neuroinflammatory environment that characterizes these disorders propagates chronic impaired function of the BBB, processes that will be discussed in this review. Limiting dysfunction of the BBB may be an attractive target for treatment of neurological disorders. To date, no current treatments are...
Source: Neurobiology of Disease - September 18, 2016 Category: Neurology Authors: de Wit NM, Vanmol J, Kamermans A, Hendriks J, de Vries HE Tags: Neurobiol Dis Source Type: research

Cellular response of the blood-brain barrier to injury: Potential biomarkers and therapeutic targets for brain regeneration.
Abstract Endothelial cells are the main component of the blood-brain barrier (BBB), a vital structure for maintaining brain homeostasis that is seriously disrupted in various neurological pathologies. Therefore, vascular-targeted therapies may bring advantages for the prevention and treatment of brain disorders. In this sense, novel methods to identify and evaluate endothelial damage have been developed and include the detection of circulating endothelial cells, endothelial progenitor cells, endothelial microparticles and exosomes. These cells and cellular structures have been documented in numerous diseases, and ...
Source: Neurobiology of Disease - March 16, 2016 Category: Neurology Authors: Tenreiro MM, Ferreira R, Bernardino L, Brito MA Tags: Neurobiol Dis Source Type: research

The carbonic anhydrase inhibitor methazolamide prevents amyloid beta-induced mitochondrial dysfunction and caspase activation protecting neuronal and glial cells in vitro and in the mouse brain.
Abstract Mitochondrial dysfunction has been recognized as an early event in Alzheimer's disease (AD) pathology, preceding and inducing neurodegeneration and memory loss. The presence of cytochrome c (CytC) released from the mitochondria into the cytoplasm is often detected after acute or chronic neurodegenerative insults, including AD. The carbonic anhydrase inhibitor (CAI) methazolamide (MTZ) was identified among a library of drugs as an inhibitor of CytC release and proved to be neuroprotective in Huntington's disease and stroke models. Here, using neuronal and glial cell cultures, in addition to an acute model ...
Source: Neurobiology of Disease - November 12, 2015 Category: Neurology Authors: Fossati S, Giannoni P, Solesio ME, Cocklin SL, Cabrera E, Ghiso J, Rostagno A Tags: Neurobiol Dis Source Type: research

The interneuron energy hypothesis: implications for brain disease.
Abstract Fast-spiking, inhibitory interneurons - prototype is the parvalbumin-positive (PV+) basket cell - generate action potentials at high frequency and synchronize the activity of numerous excitatory principal neurons, such as pyramidal cells, during fast network oscillations by rhythmic inhibition. For this purpose, fast-spiking, PV+ interneurons have unique electrophysiological characteristics regarding action potential kinetics and ion conductances, which are associated with high energy expenditure. This is reflected in the neural ultrastructure by enrichment with mitochondria and cytochrome c oxidase, indi...
Source: Neurobiology of Disease - August 15, 2015 Category: Neurology Authors: Kann O Tags: Neurobiol Dis Source Type: research

Role of HIF-1α-activated Epac1 on HSC-mediated neuroplasticity in stroke model.
We report here that hypoxia upregulated Epac1 through HIF-1α induction in the CD34-immunosorted human umbilical cord blood hematopoietic stem cells (hUCB(34)). Importantly, implantation of hUCB(34) subjected to hypoxia-preconditioning (HP-hUCB(34)) improved stroke outcome, more than did implantation of untreated hUCB(34), in rodents subjected to cerebral ischemia, and this required Epac1-to-matrix metalloproteases (MMPs) signaling. This improved therapeutic efficacy correlated with better engraftment and differentiation of these cells in the ischemic host brain. In addition, more than did implantation of untreated HP-hUCB...
Source: Neurobiology of Disease - May 20, 2013 Category: Neurology Authors: Lin CH, Lee HT, Lee SD, Lee W, Cho CW, Lin SZ, Wang HJ, Okano H, Su CY, Yu YL, Hsu CY, Shyu WC Tags: Neurobiol Dis Source Type: research