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  1. Article ; Online: Application of the Rat Grimace Scale as a Marker of Supraspinal Pain Sensation after Cervical Spinal Cord Injury.

    Schneider, Lonnie E / Henley, Kathryn Y / Turner, Omari A / Pat, Betty / Niedzielko, Tracy L / Floyd, Candace L

    Journal of neurotrauma

    2017  Volume 34, Issue 21, Page(s) 2982–2993

    Abstract: Experimental models of neuropathic pain (NP) typically rely on withdrawal responses to assess the presence of pain. Reflexive withdrawal responses to a stimulus are used to evaluate evoked pain and, as such, do not include the assessment of spontaneous ... ...

    Abstract Experimental models of neuropathic pain (NP) typically rely on withdrawal responses to assess the presence of pain. Reflexive withdrawal responses to a stimulus are used to evaluate evoked pain and, as such, do not include the assessment of spontaneous NP nor evaluation of the affective and emotional consequences of pain in animal models. Additionally, withdrawal responses can be mediated by spinal cord reflexes and may not accurately indicate supraspinal pain sensation. This is especially true in models of traumatic spinal cord injury (SCI), wherein spastic syndrome, a motor disorder characterized by exaggeration of the stretch reflex that is secondary to hyperexcitability of the spinal reflex, can cause paroxysmal withdrawals not associated with NP sensation. Consequently, the aim of this study was to utilize an assessment of supraspinal pain sensation, the Rat Grimace Scale (RGS), to measure both spontaneous and evoked NP after a contusion SCI at cervical level 5 in adult male rats. Spontaneous and evoked pain were assessed using the RGS to score facial action units before and after the application of a stimulus, respectively. Rodents exhibited significantly higher RGS scores at week 5 post-injury as compared to baseline and laminectomy controls before the application of the stimulus, suggesting the presence of spontaneous NP. Additionally, there was a significant increase in RGS scores after the application of the acetone. These data suggest that the RGS can be used to assess spontaneous NP and determine the presence of evoked supraspinal pain sensation after experimental cervical SCI.
    MeSH term(s) Animals ; Cervical Vertebrae ; Facial Expression ; Male ; Neuralgia/etiology ; Pain Measurement/methods ; Rats ; Rats, Sprague-Dawley ; Spinal Cord Injuries/complications
    Language English
    Publishing date 2017-06-26
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 645092-1
    ISSN 1557-9042 ; 0897-7151
    ISSN (online) 1557-9042
    ISSN 0897-7151
    DOI 10.1089/neu.2016.4665
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2016: Show issues Location:
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  2. Article: Nonprogressive transgene-related callosal and hippocampal changes in PDAPP mice.

    Valla, Jon / Schneider, Lonnie E / Gonzalez-Lima, Francisco / Reiman, Eric M

    Neuroreport

    2006  Volume 17, Issue 8, Page(s) 829–832

    Abstract: We have previously shown that homozygous PDAPP mice, a transgenic model of Alzheimer's-like amyloidosis, have abnormal corpus callosi and anterior hippocampi. Now, we investigated the extent to which these morphological abnormalities are correlated with ... ...

    Abstract We have previously shown that homozygous PDAPP mice, a transgenic model of Alzheimer's-like amyloidosis, have abnormal corpus callosi and anterior hippocampi. Now, we investigated the extent to which these morphological abnormalities are correlated with mutant gene dose in a larger, independent, and substantially younger cohort. Homozygous and heterozygous PDAPP mice had significantly smaller callosal commissure length and anterior hippocampal area than controls. Reductions correlated with mutant APP gene dose, with homozygotes showing the greatest reduction, and were present at 2 months of age. These findings and previous work with APP knockouts suggest that PDAPP mice have impaired white matter development due to interference with native murine APP.
    MeSH term(s) Agenesis of Corpus Callosum ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/physiopathology ; Amyloid beta-Protein Precursor/genetics ; Animals ; Corpus Callosum/metabolism ; Corpus Callosum/physiopathology ; Disease Models, Animal ; Gene Expression Regulation, Developmental/genetics ; Hippocampus/abnormalities ; Hippocampus/metabolism ; Hippocampus/physiopathology ; Male ; Mice ; Mice, Transgenic ; Mutation/genetics ; Nervous System Malformations/genetics ; Nervous System Malformations/physiopathology ; Transgenes/genetics
    Chemical Substances Amyloid beta-Protein Precursor
    Language English
    Publishing date 2006-05-29
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1049746-8
    ISSN 1473-558X ; 0959-4965
    ISSN (online) 1473-558X
    ISSN 0959-4965
    DOI 10.1097/01.wnr.0000220140.91294.15
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3118: Show issues Location:
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  3. Article ; Online: Quantitation of heteroplasmy of mtDNA sequence variants identified in a population of AD patients and controls by array-based resequencing.

    Coon, Keith D / Valla, Jon / Szelinger, Szabolics / Schneider, Lonnie E / Niedzielko, Tracy L / Brown, Kevin M / Pearson, John V / Halperin, Rebecca / Dunckley, Travis / Papassotiropoulos, Andreas / Caselli, Richard J / Reiman, Eric M / Stephan, Dietrich A

    Mitochondrion

    2006  Volume 6, Issue 4, Page(s) 194–210

    Abstract: The role of mitochondrial dysfunction in the pathogenesis of Alzheimer's disease (AD) has been well documented. Though evidence for the role of mitochondria in AD seems incontrovertible, the impact of mitochondrial DNA (mtDNA) mutations in AD etiology ... ...

    Abstract The role of mitochondrial dysfunction in the pathogenesis of Alzheimer's disease (AD) has been well documented. Though evidence for the role of mitochondria in AD seems incontrovertible, the impact of mitochondrial DNA (mtDNA) mutations in AD etiology remains controversial. Though mutations in mitochondrially encoded genes have repeatedly been implicated in the pathogenesis of AD, many of these studies have been plagued by lack of replication as well as potential contamination of nuclear-encoded mitochondrial pseudogenes. To assess the role of mtDNA mutations in the pathogenesis of AD, while avoiding the pitfalls of nuclear-encoded mitochondrial pseudogenes encountered in previous investigations and showcasing the benefits of a novel resequencing technology, we sequenced the entire coding region (15,452 bp) of mtDNA from 19 extremely well-characterized AD patients and 18 age-matched, unaffected controls utilizing a new, reliable, high-throughput array-based resequencing technique, the Human MitoChip. High-throughput, array-based DNA resequencing of the entire mtDNA coding region from platelets of 37 subjects revealed the presence of 208 loci displaying a total of 917 sequence variants. There were no statistically significant differences in overall mutational burden between cases and controls, however, 265 independent sites of statistically significant change between cases and controls were identified. Changed sites were found in genes associated with complexes I (30.2%), III (3.0%), IV (33.2%), and V (9.1%) as well as tRNA (10.6%) and rRNA (14.0%). Despite their statistical significance, the subtle nature of the observed changes makes it difficult to determine whether they represent true functional variants involved in AD etiology or merely naturally occurring dissimilarity. Regardless, this study demonstrates the tremendous value of this novel mtDNA resequencing platform, which avoids the pitfalls of erroneously amplifying nuclear-encoded mtDNA pseudogenes, and our proposed analysis paradigm, which utilizes the availability of raw signal intensity values for each of the four potential alleles to facilitate quantitative estimates of mtDNA heteroplasmy. This information provides a potential new target for burgeoning diagnostics and therapeutics that could truly assist those suffering from this devastating disorder.
    MeSH term(s) Alzheimer Disease/physiopathology ; DNA, Mitochondrial/chemistry ; DNA, Mitochondrial/genetics ; Genes, Mitochondrial ; Humans ; Mitochondria/metabolism ; Mutation ; Oligonucleotide Array Sequence Analysis/methods ; Sequence Analysis, DNA/methods
    Chemical Substances DNA, Mitochondrial
    Language English
    Publishing date 2006-08
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2056923-3
    ISSN 1872-8278 ; 1567-7249
    ISSN (online) 1872-8278
    ISSN 1567-7249
    DOI 10.1016/j.mito.2006.07.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Alzheimer's disease is associated with reduced expression of energy metabolism genes in posterior cingulate neurons.

    Liang, Winnie S / Reiman, Eric M / Valla, Jon / Dunckley, Travis / Beach, Thomas G / Grover, Andrew / Niedzielko, Tracey L / Schneider, Lonnie E / Mastroeni, Diego / Caselli, Richard / Kukull, Walter / Morris, John C / Hulette, Christine M / Schmechel, Donald / Rogers, Joseph / Stephan, Dietrich A

    Proceedings of the National Academy of Sciences of the United States of America

    2008  Volume 105, Issue 11, Page(s) 4441–4446

    Abstract: Alzheimer's disease (AD) is associated with regional reductions in fluorodeoxyglucose positron emission tomography (FDG PET) measurements of the cerebral metabolic rate for glucose, which may begin long before the onset of histopathological or clinical ... ...

    Abstract Alzheimer's disease (AD) is associated with regional reductions in fluorodeoxyglucose positron emission tomography (FDG PET) measurements of the cerebral metabolic rate for glucose, which may begin long before the onset of histopathological or clinical features, especially in carriers of a common AD susceptibility gene. Molecular evaluation of cells from metabolically affected brain regions could provide new information about the pathogenesis of AD and new targets at which to aim disease-slowing and prevention therapies. Data from a genome-wide transcriptomic study were used to compare the expression of 80 metabolically relevant nuclear genes from laser-capture microdissected non-tangle-bearing neurons from autopsy brains of AD cases and normal controls in posterior cingulate cortex, which is metabolically affected in the earliest stages; other brain regions metabolically affected in PET studies of AD or normal aging; and visual cortex, which is relatively spared. Compared with controls, AD cases had significantly lower expression of 70% of the nuclear genes encoding subunits of the mitochondrial electron transport chain in posterior cingulate cortex, 65% of those in the middle temporal gyrus, 61% of those in hippocampal CA1, 23% of those in entorhinal cortex, 16% of those in visual cortex, and 5% of those in the superior frontal gyrus. Western blots confirmed underexpression of those complex I-V subunits assessed at the protein level. Cerebral metabolic rate for glucose abnormalities in FDG PET studies of AD may be associated with reduced neuronal expression of nuclear genes encoding subunits of the mitochondrial electron transport chain.
    MeSH term(s) Aged ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Brain/metabolism ; Energy Metabolism ; Female ; Gene Expression Regulation/genetics ; Humans ; Male ; Neurons/metabolism
    Language English
    Publishing date 2008-03-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.0709259105
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: Show issues Location:
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  5. Article: Alzheimer's disease is associated with reduced expression of energy metabolism genes in posterior cingulate neurons

    Liang, Winnie S / Reiman, Eric M / Valla, Jon / Dunckley, Travis / Beach, Thomas G / Grover, Andrew / Niedzielko, Tracey L / Schneider, Lonnie E / Mastroeni, Diego / Caselli, Richard / Kukull, Walter / Morris, John C / Hulette, Christine M / Schmechel, Donald / Rogers, Joseph / Stephan, Dietrich A

    Proceedings of the National Academy of Sciences of the United States of America. 2008 Mar. 18, v. 105, no. 11

    2008  

    Abstract: Alzheimer's disease (AD) is associated with regional reductions in fluorodeoxyglucose positron emission tomography (FDG PET) measurements of the cerebral metabolic rate for glucose, which may begin long before the onset of histopathological or clinical ... ...

    Abstract Alzheimer's disease (AD) is associated with regional reductions in fluorodeoxyglucose positron emission tomography (FDG PET) measurements of the cerebral metabolic rate for glucose, which may begin long before the onset of histopathological or clinical features, especially in carriers of a common AD susceptibility gene. Molecular evaluation of cells from metabolically affected brain regions could provide new information about the pathogenesis of AD and new targets at which to aim disease-slowing and prevention therapies. Data from a genome-wide transcriptomic study were used to compare the expression of 80 metabolically relevant nuclear genes from laser-capture microdissected non-tangle-bearing neurons from autopsy brains of AD cases and normal controls in posterior cingulate cortex, which is metabolically affected in the earliest stages; other brain regions metabolically affected in PET studies of AD or normal aging; and visual cortex, which is relatively spared. Compared with controls, AD cases had significantly lower expression of 70% of the nuclear genes encoding subunits of the mitochondrial electron transport chain in posterior cingulate cortex, 65% of those in the middle temporal gyrus, 61% of those in hippocampal CA1, 23% of those in entorhinal cortex, 16% of those in visual cortex, and 5% of those in the superior frontal gyrus. Western blots confirmed underexpression of those complex I-V subunits assessed at the protein level. Cerebral metabolic rate for glucose abnormalities in FDG PET studies of AD may be associated with reduced neuronal expression of nuclear genes encoding subunits of the mitochondrial electron transport chain.
    Language English
    Dates of publication 2008-0318
    Size p. 4441-4446.
    Publishing place National Academy of Sciences
    Document type Article
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    Database NAL-Catalogue (AGRICOLA)

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