HIV-associated dementia, Alzheimer's disease, multiple sclerosis, and schizophrenia: gene expression review

Minagar, Alireza; Shapshak, Paul; Duran, Elda M.; Kablinger, Anita S.; Alexander, Jeff; Kelley, Roger E.; Seth, Raman; Kazic, Toni

doi:10.1016/j.jns.2004.06.007

Cited by 18 publications

(11 citation statements)

References 84 publications

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“…These inflammatory mediators promote inflammatory signaling cascades in NeuroAIDS with a cumulative result of neuronal toxicity [49,136–138]. TNF-α levels increase in the CNS of patients with HAND and in-vitro exposure of macrophages and microglia to gp120 or Tat induces TNF-1α expression [139].…”

Section: Molecularmentioning

confidence: 99%

“…In human astrocyte cultures, activation of indoleamine-2,3-dioxygenase (IDO) results in elevation of tryptophan catabolism and the production of neurotoxins including kynurenine due to Tat protein for HIV-1B and not C. The authors conclude from the latter experiment that the prevalence of HAD may correlate with epidemiological differences in HIV-1B vs. C [139,145–148]. Finally, microarray technology has been applied to NeuroAIDS to measure simultaneous expression of large numbers of genes including recently discovered micro-(mi)-RNAs, as reviewed in detail elsewhere (Table 3) [49,50,96,136,138,140,141,145–154]. …”

Section: Molecularmentioning

confidence: 99%

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Editorial NeuroAIDS review

Shapshak

Kangueane

Fujimura

et al. 2011

Aids

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Section: Molecularmentioning

confidence: 99%

Section: Molecularmentioning

confidence: 99%

Editorial NeuroAIDS review

Shapshak

Kangueane

Fujimura

et al. 2011

Aids

Self Cite

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“…In each selected clinical study (Table 2), a correlation can be made between an adverse or high-risk association, a low-risk or protective effect, or no association relative to the ApoE genotype. For example, hepatitis B (Percy et al, 2003), multiple sclerosis (Minagar et al, 2004), Huntington's disease (Saft et al, 2004), and Parkinson's disease (Hemling et al, 2003) are conditions in which, to date, no association or risk factor involvement has been proven to exist between any ApoE genotype and disease severity or protection. While it is assumed that these diseases are not related to the presence or absence of specific ApoE alleles, in any clinical condition, subsets of clinical patients and more stringent definitions might identify an association.…”

Section: Chemistry and Genetics Of Human Apoementioning

confidence: 99%

“…As noted in Table 2, there are suggested associations between AD, ApoE alleles, and HSV-1. The ε 4/ε 4 allele has also been reported to reduce the severity of hepatitis C but not onset, whereas with HIV infections, the ε 4/ε 4 allele increases the severity both of the infection and dementia (Corder et al, 1998b;Minagar et al, 2004;Mueller et al, 2003;Toniutto et al, 2004;Wozniak et al, 2002).…”

Section: Chemistry and Genetics Of Human Apoementioning

confidence: 99%

Apolipoprotein E alleles can contribute to the pathogenesis of numerous clinical conditions including HSV-1 corneal disease

Hill

Bhattacharjee

Neumann

2007

Experimental Eye Research

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Apolipoprotein E (ApoE) alleles have been reported to affect the clinical outcome of numerous cardiovascular, neurodegenerative, and viral infectious diseases, including atherosclerosis, Alzheimer's disease (AD), hepatitis C, and HIV. The major alleles of ApoE are ε 2, ε 3, and ε 4. ApoE genotypes have been hypothesized to regulate many biological functions, resulting in significant changes in the onset and/or outcome (severity and duration) of several clinical conditions. Based on genetic analyses in human and animal studies using knockout (ApoE −/−) mice and mice transgenic for human ε 3 and ε 4, we present evidence that strongly suggests that the ApoE alleles can regulate the pathogenesis of ocular herpes simplex virus type 1 (HSV-1) infections. This review will summarize the major studies that support this hypothesis. Significant gender based differences in HSV-1 pathogenesis have also been reported, suggesting that hormonal regulation combined with ApoE genotype plays a significant role in HSV-1 pathogenesis. Identification of specific mechanisms in ocular HSV-1 infections related to the ApoE alleles and gender could lead to therapeutic intervention based on the properties of the apoE isoforms. While many clinical investigations have been reported and, to a lesser extent, transgenic mouse studies have been conducted, no specific mechanisms of how ApoE induces or alters clinical disease are known.

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“…Regional analysis of gene expression is a widely used paradigm because of the relatively large amounts of RNA that can be extracted from carefully dissected frozen animal model tissues as well as postmortem human brain tissues, as evidenced by reports on amyloid overexpression 105,106 and several neurodegenerative disorders, including AD. [107][108][109][110][111][112][113][114][115][116] An advantage of regional gene expression analysis is that, in most cases, extracted RNA is sufficient to generate significant hybridization signal intensity for microarray analysis, enabling the analysis of thousands of targets without necessitating RNA amplification protocols. However, expression profiles garnered from regional dissections cannot discern molecular signatures in discrete neuronal populations nor can regional assessments evaluate differences in admixed neuronal and nonneuronal populations.…”

Section: Regional Assessments Of Gene Expression In the Ad Brainmentioning

confidence: 99%

Single cell gene expression profiling in Alzheimer’s disease

et al. 2006

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Summary: Development and implementation of microarray techniques to quantify expression levels of dozens to hundreds to thousands of transcripts simultaneously within select tissue samples from normal control subjects and neurodegenerative diseased brains has enabled scientists to create molecular fingerprints of vulnerable neuronal populations in Alzheimer's disease (AD) and related disorders. A goal is to sample gene expression from homogeneous cell types within a defined region without potential contamination by expression profiles of adjacent neuronal subpopulations and nonneuronal cells. The precise resolution afforded by single cell and population cell RNA analysis in combination with microarrays and real-time quantitative polymerase chain reaction (qPCR)-based analyses allows for relative gene expression level comparisons across cell types under different experimental conditions and disease progression. The ability to analyze single cells is an important distinction from global and regional assessments of mRNA expression and can be applied to optimally prepared tissues from animal models of neurodegeneration as well as postmortem human brain tissues. Gene expression analysis in postmortem AD brain regions including the hippocampal formation and neocortex reveals selectively vulnerable cell types share putative pathogenetic alterations in common classes of transcripts, for example, markers of glutamatergic neurotransmission, synaptic-related markers, protein phosphatases and kinases, and neurotrophins/neurotrophin receptors. Expression profiles of vulnerable regions and neurons may reveal important clues toward the understanding of the molecular pathogenesis of various neurological diseases and aid in identifying rational targets toward pharmacotherapeutic interventions for progressive, late-onset neurodegenerative disorders such as mild cognitive impairment (MCI) and AD.

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HIV-associated dementia, Alzheimer's disease, multiple sclerosis, and schizophrenia: gene expression review

Cited by 18 publications

References 84 publications

Editorial NeuroAIDS review

Editorial NeuroAIDS review

Apolipoprotein E alleles can contribute to the pathogenesis of numerous clinical conditions including HSV-1 corneal disease

Single cell gene expression profiling in Alzheimer’s disease

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