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Faculty Detail     Name INGA KADISHA   Campus Address THT 912 Zip 0006 Phone 205-934-5940 E-mail ikadisha@uab.edu Other websites http://main.uab.edu/show.asp?durki=107708

Faculty Appointment(s) Appointment Type Department Division Rank Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Assistant Professor Center  Center for Aging  Center for Aging Assistant Professor Center  General Clinical Research Center  Comprehensive Neuroscience Center Assistant Professor Center  Ctr for Glial Bio in Med  Ctr for Glial Bio in Med Assistant Professor Center  Neurology   Ctr Neurodegeneration & Exp Ther (CNET) Assistant Professor

Graduate Biomedical Sciences Affiliations Neuroscience  Pathobiology and Molecular Medicine

Biographical Sketch  University of Latvia, Latvia MS 06/85 Human/ Animal Physiology University of Kuopio, Finland PhD 06/02 Neuroscience/Neurology University of Kuopio, Finland Post-doc 07/02-01/04 Neuroscience Univ. of Alabama at Birmingham, USA Post-doc 02/04-06/06 Hypertension/Vascular Biology

Society Memberships Organization Name Position Held Org Link EBBS  member  http://www.ebbs-science.org/cms/  Society for Neuroscience  member  http://www.sfn.org/

Research/Clinical Interest Title The role of white matter changes in aging and Alzheimer's disease Description The overall goal of my research is to elucidate the role of white matter pathology in the development of age-related cognitive deficits. Currently, our studies have shown two significant changes in white matter pathology with aging malfunctioning of oligodendrocytes and demyelination of axons. Further, cholesterol trafficking is disturbed early in the aging process in the white matter, specifically in astrocytes, and since astrocytes are the main source of cholesterol in the brain, this likely leads to changes in the myelin sheath. Together these changes will lead to a “functional” disconnection in the brain leading to cognitive disturbances. We are investigating these changes in oligodendrocyte dysfunction in the white matter, and the development of cognitive impairments, using a combination of behavioral, immunohistochemical and molecular biology approaches. Furthermore, we have recently discovered changes in the expression of epigenetic markers with aging, i.e., changes in HDACs and DNMTs in the white matter. This novel discovery has lead to potential new therapies for age-related white matter pathology. A second research interest is the role of vascular pathology in Alzheimer’s disease, specifically hypertension and the relation between white matter infarcts and AD pathology. While clinical data strongly suggest that small infarcts contribute significantly to cognitive decline, the causal relationship is still not clearly defined. Our studies have shown that small ischemic infarcts both increase Aß deposition and decrease cognition. Furthermore, we have found that white matter infarcts (compared to grey matter infarcts) have a significantly worse outcome. Currently we are focusing on the role of hypertension in age-related cerebral dysfunction and Alzheimer’s disease. Some of my current studies include the use of therapeutic agents (i.e., amyloid β binding peptides) that may be promising in the alleviation or delay of age-related neural and cognitive changes. Further, currently, we are investigating the role of obesity, and/or caloric restriction and hunger in the development of cognitive deficits in AD.

Selected Publications  Publication PUBMEDID Long-Term Pioglitazone Treatment Improves Learning and Attenuates Pathological Markers in a Mouse Model of Alzheimer's Disease. Searcy JL, Phelps JT, Pancani T, Kadish I, Popovic J, Anderson KL, Beckett TL, Murphy MP, Chen KC, Blalock EM, Landfield PW, Porter NM, Thibault O. J Alzheimers Dis. 2012 Apr 10. [Epub ahead of print]   22495349  Disrupting function of FK506-binding protein 1b/12.6 induces the Ca²+-dysregulation aging phenotype in hippocampal neurons. Gant JC, Chen KC, Norris CM, Kadish I, Thibault O, Blalock EM, Porter NM, Landfield PW. J Neurosci. 2011 Feb 2;31(5):1693-703   21289178  Transgenic AD model mice, effects of potential anti-AD treatments on inflammation, and pathology. van Groen T, Miettinen P, Kadish I. J Alzheimers Dis. 2011;24(2):301-13.   21239852  Age-related brain pathology in Octodon degu: blood vessel, white matter and Alzheimer-like pathology. van Groen T, Kadish I, Popović N, Popović M, Caballero-Bleda M, Baño-Otálora B, Vivanco P, Rol MÁ, Madrid JA. Neurobiol Aging. 2011 Sep;32(9):1651-61. Epub 2009 Nov 11.   19910078  Lesion-induced hippocampal plasticity in transgenic Alzheimer's disease mouse models: influences of age, genotype, and estrogen. Kadish I, van Groen T. J Alzheimers Dis. 2009;18(2):429-45.   19584452  Oral apolipoprotein A-I mimetic peptide improves cognitive function and reduces amyloid burden in a mouse model of Alzheimer's disease. Handattu SP, Garber DW, Monroe CE, van Groen T, Kadish I, Nayyar G, Cao D, Palgunachari MN, Li L, Anantharamaiah GM. Neurobiol Dis. 2009 Jun;34(3):525-34. Epub 2009 Apr 1.   19344763  Hippocampal and cognitive aging across the lifespan: a bioenergetic shift precedes and increased cholesterol trafficking parallels memory impairment. Kadish I, Thibault O, Blalock EM, Chen KC, Gant JC, Porter NM, Landfield PW. J Neurosci. 2009 Feb 11;29(6):1805-16.   19211887  Pulmonary angiogenesis in a rat model of hepatopulmonary syndrome. Zhang J, Luo B, Tang L, Wang Y, Stockard CR, Kadish I, Van Groen T, Grizzle WE, Ponnazhagan S, Fallon MB. Gastroenterology. 2009 Mar;136(3):1070-80. Epub 2008 Dec 3.   19109954  In vitro and in vivo staining characteristics of small, fluorescent, Abeta42-binding D-enantiomeric peptides in transgenic AD mouse models. van Groen T, Kadish I, Wiesehan K, Funke SA, Willbold D. ChemMedChem. 2009 Feb;4(2):276-82.   19072935  Reduction of Alzheimer's disease amyloid plaque load in transgenic mice by D3, A D-enantiomeric peptide identified by mirror image phage display. van Groen T, Wiesehan K, Funke SA, Kadish I, Nagel-Steger L, Willbold D. ChemMedChem. 2008 Dec;3(12):1848-52.   19016284  First Prev   1 2 3 of  3  Next Last

Keywords Alzheimer's Disease, Aging, Cognition

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