Rescue of adult hippocampal neurogenesis in a mouse model of HIV neurologic disease.

Abstract:

:The prevalence of central nervous system (CNS) neurologic dysfunction associated with human immunodeficiency virus (HIV) infection continues to increase, despite the use of antiretroviral therapy. Previous work has focused on the deleterious effects of HIV on mature neurons and on development of neuroprotective strategies, which have consistently failed to show a meaningful clinical benefit. It is now well established that new neurons are continuously generated in discrete regions in the adult mammalian brain, and accumulating evidence supports important roles for these neurons in specific cognitive functions. In a transgenic mouse model of HIV neurologic disease with glial expression of the HIV envelope protein gp120, we demonstrate a significant reduction in proliferation of hippocampal neural progenitors in the dentate gyrus of adult animals, resulting in a dramatic decrease in the number of newborn neurons in the adult brain. We identify amplifying neural progenitor cells (ANPs) as the first class of progenitors affected by gp120, and we also demonstrate that newly generated neurons exhibit aberrant dendritic development. Furthermore, voluntary exercise and treatment with a selective serotonin reuptake inhibitor increase the ANP population and rescue the observed deficits in gp120 transgenic mice. Thus, during HIV infection, the envelope protein gp120 may potently inhibit adult hippocampal neurogenesis, and neurorestorative approaches may be effective in ameliorating these effects. Our study has significant implications for the development of novel therapeutic approaches for HIV-infected individuals with neurologic dysfunction and may be applicable to other neurodegenerative diseases in which hippocampal neurogenesis is impaired.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Lee MH,Wang T,Jang MH,Steiner J,Haughey N,Ming GL,Song H,Nath A,Venkatesan A

doi

10.1016/j.nbd.2010.12.002

subject

Has Abstract

pub_date

2011-03-01 00:00:00

pages

678-87

issue

3

eissn

0969-9961

issn

1095-953X

pii

S0969-9961(10)00395-5

journal_volume

41

pub_type

杂志文章
  • The role of REST in transcriptional and epigenetic dysregulation in Huntington's disease.

    abstract::Huntington's disease (HD) is a devastating disorder that affects approximately 1 in 10,000 people and is accompanied by neuronal dysfunction and neurodegeneration. HD manifests as a progressive chorea, a decline in mental abilities accompanied by behavioural, emotional and psychiatric problems followed by, dementia, a...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章,评审

    doi:10.1016/j.nbd.2010.02.003

    authors: Buckley NJ,Johnson R,Zuccato C,Bithell A,Cattaneo E

    更新日期:2010-07-01 00:00:00

  • A human single-chain Fv intrabody preferentially targets amino-terminal Huntingtin's fragments in striatal models of Huntington's disease.

    abstract::Amino-terminal fragments of huntingtin (htt) appear to result from proteolytic processing of the full-length protein in Huntington's disease (HD), and fragments containing pathological expansions of polyglutamine elicit toxicity in model systems. Such fragments are sequestered into insoluble aggregates, which may init...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2004.11.003

    authors: Miller TW,Zhou C,Gines S,MacDonald ME,Mazarakis ND,Bates GP,Huston JS,Messer A

    更新日期:2005-06-01 00:00:00

  • In vivo imaging reveals impaired connectivity across cortical and subcortical networks in a mouse model of DYT1 dystonia.

    abstract::Developing in vivo functional and structural neuroimaging assays in Dyt1 ΔGAG heterozygous knock-in (Dyt1 KI) mice provide insight into the pathophysiology underlying DYT1 dystonia. In the current study, we examined in vivo functional connectivity of large-scale cortical and subcortical networks in Dyt1 KI mice and wi...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2016.07.005

    authors: DeSimone JC,Febo M,Shukla P,Ofori E,Colon-Perez LM,Li Y,Vaillancourt DE

    更新日期:2016-11-01 00:00:00

  • Developmental expression of GPR3 in rodent cerebellar granule neurons is associated with cell survival and protects neurons from various apoptotic stimuli.

    abstract::G-protein coupled receptor 3 (GPR3), GPR6, and GPR12 belong to a family of constitutively active Gs-coupled receptors that activate 3'-5'-cyclic adenosine monophosphate (cAMP) and are highly expressed in the brain. Among these receptors, the endogenous expression of GPR3 in cerebellar granule neurons (CGNs) is increas...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2014.04.007

    authors: Tanaka S,Miyagi T,Dohi E,Seki T,Hide I,Sotomaru Y,Saeki Y,Antonio Chiocca E,Matsumoto M,Sakai N

    更新日期:2014-08-01 00:00:00

  • Maternal immune activation impairs cognitive flexibility and alters transcription in frontal cortex.

    abstract:BACKGROUND:Epidemiological studies suggest that the risk of neurodevelopmental disorders such as autism spectrum disorder (ASD) and schizophrenia is increased by prenatal exposure to viral or bacterial infection during pregnancy. It is still unclear how activation of the maternal immune response interacts with underlyi...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2019.01.025

    authors: Amodeo DA,Lai CY,Hassan O,Mukamel EA,Behrens MM,Powell SB

    更新日期:2019-05-01 00:00:00

  • Beta-amyloid controls altered Reelin expression and processing in Alzheimer's disease.

    abstract::Reelin is a glycoprotein that modulates synaptic function and plasticity in the mature brain, thereby favouring memory formation. We recently reported altered cerebral Reelin expression in Alzheimer's disease (AD). Here we demonstrate pronounced Reelin changes at protein and mRNA levels in the frontal cortex in adult ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2009.12.006

    authors: Botella-López A,Cuchillo-Ibáñez I,Cotrufo T,Mok SS,Li QX,Barquero MS,Dierssen M,Soriano E,Sáez-Valero J

    更新日期:2010-03-01 00:00:00

  • Gene co-expression networks shed light into diseases of brain iron accumulation.

    abstract::Aberrant brain iron deposition is observed in both common and rare neurodegenerative disorders, including those categorized as Neurodegeneration with Brain Iron Accumulation (NBIA), which are characterized by focal iron accumulation in the basal ganglia. Two NBIA genes are directly involved in iron metabolism, but whe...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2015.12.004

    authors: Bettencourt C,Forabosco P,Wiethoff S,Heidari M,Johnstone DM,Botía JA,Collingwood JF,Hardy J,UK Brain Expression Consortium (UKBEC).,Milward EA,Ryten M,Houlden H

    更新日期:2016-03-01 00:00:00

  • Adolescent cannabis exposure interacts with mutant DISC1 to produce impaired adult emotional memory.

    abstract::Cannabis is an increasingly popular and controversial drug used worldwide. Cannabis use often begins during adolescence, a highly susceptible period for environmental stimuli to alter functional and structural organization of the developing brain. Given that adolescence is a critical time for the emergence of mental i...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2015.06.006

    authors: Ballinger MD,Saito A,Abazyan B,Taniguchi Y,Huang CH,Ito K,Zhu X,Segal H,Jaaro-Peled H,Sawa A,Mackie K,Pletnikov MV,Kamiya A

    更新日期:2015-10-01 00:00:00

  • Hyperleucinemia causes hippocampal retromer deficiency linking diabetes to Alzheimer's disease.

    abstract::Type 2 diabetes (T2D) is a major risk factor for late-onset Alzheimer's disease (AD). A variety of metabolic changes related to T2D (e.g. hyperinsulinemia, hyperglycemia, and elevated branched-chain amino acids) have been proposed as mechanistic links, but the basis for this association remains unknown. Retromer-depen...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2013.12.017

    authors: Morabito MV,Berman DE,Schneider RT,Zhang Y,Leibel RL,Small SA

    更新日期:2014-05-01 00:00:00

  • Purkinje cell-specific Grip1/2 knockout mice show increased repetitive self-grooming and enhanced mGluR5 signaling in cerebellum.

    abstract::Cerebellar Purkinje cell (PC) loss is a consistent pathological finding in autism. However, neural mechanisms of PC-dysfunction in autism remain poorly characterized. Glutamate receptor interacting proteins 1/2 (Grip1/2) regulate AMPA receptor (AMPAR) trafficking and synaptic strength. To evaluate role of PC-AMPAR sig...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2019.104602

    authors: Mejias R,Chiu SL,Han M,Rose R,Gil-Infante A,Zhao Y,Huganir RL,Wang T

    更新日期:2019-12-01 00:00:00

  • Astrocytic expression of the chaperone DNAJB6 results in non-cell autonomous protection in Huntington's disease.

    abstract::Several neurodegenerative diseases like Huntington's, a polyglutamine (PolyQ) disease, are initiated by protein aggregation in neurons. Furthermore, these diseases are also associated with a multitude of responses in non-neuronal cells in the brain, in particular glial cells, like astrocytes. These non-neuronal respon...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2018.10.017

    authors: Bason M,Meister-Broekema M,Alberts N,Dijkers P,Bergink S,Sibon OCM,Kampinga HH

    更新日期:2019-04-01 00:00:00

  • Apolipoprotein E-low density lipoprotein receptor interaction affects spatial memory retention and brain ApoE levels in an isoform-dependent manner.

    abstract::Human apolipoprotein E (apoE) exists in three isoforms: apoE2, apoE3 and apoE4. APOE ε4 is a major genetic risk factor for cardiovascular disease (CVD) and Alzheimer's disease (AD). ApoE mediates cholesterol metabolism by binding various receptors. The low-density lipoprotein receptor (LDLR) has a high affinity for ap...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2013.12.016

    authors: Johnson LA,Olsen RH,Merkens LS,DeBarber A,Steiner RD,Sullivan PM,Maeda N,Raber J

    更新日期:2014-04-01 00:00:00

  • Frontotemporal dementia and mitochondrial DNA transitions.

    abstract::Frontotemporal dementia (FTD) is the second most common type of primary degenerative dementia. Some patients present an overlap between Alzheimer's disease (AD) and FTD both in neuropathological and clinical aspects. This may suggest a similar overlap in physiopathology, namely an involvement of mitochondrial DNA (mtD...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2003.11.004

    authors: Grazina M,Silva F,Santana I,Santiago B,Mendes C,Simões M,Oliveira M,Cunha L,Oliveira C

    更新日期:2004-03-01 00:00:00

  • Dual response of BDNF to sublethal concentrations of beta-amyloid peptides in cultured cortical neurons.

    abstract::Beta-amyloid (Abeta) deposition is one important pathological hallmark in Alzheimer's disease (AD). However, low levels of Abeta may modify critical endogenous protection systems before neurodegeneration occurs. We examined the time-course effect of sublethal concentrations of Abeta on total BDNF (panBDNF), BDNF trans...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2009.10.004

    authors: Aliaga E,Silhol M,Bonneau N,Maurice T,Arancibia S,Tapia-Arancibia L

    更新日期:2010-01-01 00:00:00

  • Locomotor hyperactivity and alterations in dopamine neurotransmission are associated with overexpression of A53T mutant human alpha-synuclein in mice.

    abstract::Genetic and biochemical abnormalities associated with alpha-synuclein are implicated in the etiology of Parkinson's disease (PD). In this study, altered locomotor behavior linked to the expression of mutant or wildtype human alpha-synuclein was investigated. A53T alpha-synuclein transgenic (A53T-tg) mice exhibited nor...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2005.08.005

    authors: Unger EL,Eve DJ,Perez XA,Reichenbach DK,Xu Y,Lee MK,Andrews AM

    更新日期:2006-02-01 00:00:00

  • Neutral sphingomyelinase activation in endothelial and glial cell death induced by amyloid beta-peptide.

    abstract::We have explored the molecular mechanism underlying amyloid beta-peptide (Abeta)-mediated cytotoxicity in vitro. Exposure of murine cerebral endothelial cells (CECs) or C6 glioma cells to Abeta25-35 resulted in dose-dependent cell death. Ceramide is a pro-apoptotic lipid mediator. Forced elevation of cellular ceramide...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2004.06.001

    authors: Yang DI,Yeh CH,Chen S,Xu J,Hsu CY

    更新日期:2004-10-01 00:00:00

  • Platform influence on DNA microarray data in postmortem brain research.

    abstract::In addition to the substantial biological diversity among humans, our limited ability to reliably measure expression changes of small magnitude significantly reduces our capacity to obtain convergent sets of transcriptome data in postmortem brain. In particular, differences in the structure and sensitivity/reproducibi...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2004.10.020

    authors: Hollingshead D,Lewis DA,Mirnics K

    更新日期:2005-04-01 00:00:00

  • TAT-Bcl-x(L) improves survival of neuronal precursor cells in the lesioned striatum after focal cerebral ischemia.

    abstract::Cerebral ischemia activates endogenous neurogenesis in the subventricular zone (SVZ) and the dentate gyrus. Consecutively, SVZ-derived neural precursors migrate towards ischemic lesions. However, functional relevance of activated neurogenesis is limited by poor survival of new-born precursors. We therefore employed th...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2008.12.013

    authors: Doeppner TR,Dietz GP,El Aanbouri M,Gerber J,Witte OW,Bähr M,Weise J

    更新日期:2009-04-01 00:00:00

  • Genetically determined susceptibility to neurodegeneration is associated with expression of inflammatory genes.

    abstract::Axonal damage, a core feature of neurological diseases, induces a retrograde reaction in neurons and surrounding glia. We determined transcriptional profiles of this reaction using Affymetrix oligonucleotide arrays. Gene expression was examined in spinal cord tissue prior to injury and following ventral root avulsion ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2006.05.016

    authors: Swanberg M,Duvefelt K,Diez M,Hillert J,Olsson T,Piehl F,Lidman O

    更新日期:2006-10-01 00:00:00

  • Effects of chronic network hyperexcitability on the growth of hippocampal dendrites.

    abstract::Experiments reported here were motivated by studies in both human epilepsy and animal models in which stunted dendritic arbors are observed. Our goal was to determine if chronic network hyperexcitability alters dendritic growth. Experiments were conducted in hippocampal slice cultures obtained from infant mice that ex...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2007.08.018

    authors: Nishimura M,Owens J,Swann JW

    更新日期:2008-02-01 00:00:00

  • Polyglutamine-induced neurodegeneration in SCA3 is not mitigated by non-expanded ataxin-3: conclusions from double-transgenic mouse models.

    abstract::A crucial question in polyQ-induced neurodegeneration is the influence of wild type protein on the formation of aggregates and toxicity. Recently it was shown that non-expanded ataxin-3 protein mitigated neurodegeneration in a Drosophila and mouse model of SCA3. We now explored the effects of overexpressing non-expand...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2010.01.005

    authors: Hübener J,Riess O

    更新日期:2010-04-01 00:00:00

  • Identification of candidate proteins binding to prion protein.

    abstract::Prion diseases are disorders of protein conformation that produce neurodegeneration in humans and animals. Studies of transgenic (Tg) mice indicate that a factor designated protein X is involved in the conversion of the normal cellular prion protein (PrPC) into the scrapie isoform (PrPSc); protein X appears to interac...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1006/nbdi.1997.0130

    authors: Yehiely F,Bamborough P,Da Costa M,Perry BJ,Thinakaran G,Cohen FE,Carlson GA,Prusiner SB

    更新日期:1997-01-01 00:00:00

  • Increased mortality and spatial memory deficits in TNF-alpha-deficient mice in ceftriaxone-treated experimental pneumococcal meningitis.

    abstract::Tumor necrosis factor-alpha (TNF-alpha) is critically involved in inflammation and may participate in hippocampal injury in bacterial meningitis. In a mouse model of ceftriaxone-treated pneumococcal meningitis, spatial memory and motor performance of TNF-alpha-deficient (n = 57) and control mice (n = 55) were investig...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2004.01.013

    authors: Gerber J,Böttcher T,Hahn M,Siemer A,Bunkowski S,Nau R

    更新日期:2004-06-01 00:00:00

  • Unraveling substantia nigra sequential gene expression in a progressive MPTP-lesioned macaque model of Parkinson's disease.

    abstract::Taking advantage of a progressive nonhuman primate model mimicking Parkinson's disease (PD) evolution, we monitored transcriptional fluctuations in the substantia nigra using Affymetrix microarrays in control (normal), saline-treated (normal), 6 days-treated (asymptomatic with 20% cell loss), 12 days-treated (asymptom...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2005.02.005

    authors: Bassilana F,Mace N,Li Q,Stutzmann JM,Gross CE,Pradier L,Benavides J,Ménager J,Bezard E

    更新日期:2005-10-01 00:00:00

  • Functional MAPT haplotypes: bridging the gap between genotype and neuropathology.

    abstract::The microtubule-associated protein tau (MAPT) locus has long been associated with sporadic neurodegenerative disease, notably progressive supranuclear palsy and corticobasal degeneration, and more recently with Alzheimer's disease and Parkinson's disease. However, the functional biological mechanisms behind the geneti...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章,评审

    doi:10.1016/j.nbd.2007.04.006

    authors: Caffrey TM,Wade-Martins R

    更新日期:2007-07-01 00:00:00

  • TAT-mediated delivery of Bcl-xL protein is neuroprotective against neonatal hypoxic-ischemic brain injury via inhibition of caspases and AIF.

    abstract::Systemic delivery of recombinant Bcl-xL fusion protein containing the TAT protein transduction domain attenuated neonatal brain damage following hypoxic ischemia (H-I). Within 30 min after intraperitoneal injection of TAT-Bcl-xL protein into 7-day-old rats, substantially enhanced levels of Bcl-xL were found in several...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2005.07.015

    authors: Yin W,Cao G,Johnnides MJ,Signore AP,Luo Y,Hickey RW,Chen J

    更新日期:2006-02-01 00:00:00

  • Transgenic expression of an expanded (GCG)13 repeat PABPN1 leads to weakness and coordination defects in mice.

    abstract::Oculopharyngeal muscular dystrophy (OPMD) is a late-onset disorder caused by a (GCG)n trinucleotide repeat expansion in the poly(A) binding protein nuclear-1 (PABPN1) gene, which in turn leads to an expanded polyalanine tract in the protein. We generated transgenic mice expressing either the wild type or the expanded ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2004.09.021

    authors: Dion P,Shanmugam V,Gaspar C,Messaed C,Meijer I,Toulouse A,Laganiere J,Roussel J,Rochefort D,Laganiere S,Allen C,Karpati G,Bouchard JP,Brais B,Rouleau GA

    更新日期:2005-04-01 00:00:00

  • Post-seizures amygdaloallocortical microvascular lesion leading to atrophy and memory impairment.

    abstract::Although the incidence of seizures after a cerebrovascular event including intracerebral hemorrhage has been widely recognized, the present studies have demonstrated that generalized convulsive seizures can cause multifocal amygdaloallocortical hemorrhage and tissue necrosis, the origin of which remains to be establis...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2005.01.029

    authors: Mraovitch S,Calando Y,Régnier A,Lamproglou I,Vicaut E

    更新日期:2005-08-01 00:00:00

  • Hyperphosphorylated tau and paired helical filament-like structures in the brains of mice carrying mutant amyloid precursor protein and mutant presenilin-1 transgenes.

    abstract::Senile plaques composed mainly of beta-amyloid (Abeta) and neurofibrillary tangles principally composed of hyperphosphorylated tau are the major pathological features of Alzheimer's disease (AD). Despite the fact that increased expression of amyloid precursor protein (APP) and presenilin-1 (PS1) transgenes in mice lea...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/s0969-9961(03)00084-6

    authors: Kurt MA,Davies DC,Kidd M,Duff K,Howlett DR

    更新日期:2003-10-01 00:00:00

  • Phenothiazines interfere with dopaminergic neurodegeneration in Caenorhabditis elegans models of Parkinson's disease.

    abstract::Oxidative stress is involved in the pathogenesis of various neurodegenerative disorders, conventional antioxidant strategies have yet been of limited success. We have employed transgenic Caenorhabditis elegans expressing DsRed2 in dopaminergic neurons and CFP pan-neuronally, to characterize in larval and adult animals...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2010.03.019

    authors: Mocko JB,Kern A,Moosmann B,Behl C,Hajieva P

    更新日期:2010-10-01 00:00:00