Grant Detail
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Subgroups of Alzheimer Disease
15 May 2007 - 30 April 2012
NATIONAL INSTITUTE ON AGING
Total Funding: $ 1,630,946
DESCRIPTION (provided by applicant): The overall objective of this proposal is to investigate the nature of different signaling pathways involved in the etiopathogenesis of neurofibrillary degeneration of abnormally hyperphosphorylated tau, a hallmark brain lesion of Alzheimer disease (AD), Down syndrome, frontotemporal dementia, and other tauopathies, and employ this information to identify and diagnose the different subgroups of Alzheimer's disease. We postulate that more than one disease mechanism and signaling pathway are involved in producing AD pathology, and that various subgroups of this disease can be identified based on CSF levels of proteins associated with plaques and neurofibrillary tangles and of taus abnormally phosphorylated at various specific sites. To test this hypothesis we propose (1) to develop and validate ultrasensitive bienzyme-recycle ELISAs for various abnormal phosphorylation sites of tau. (2) To determine CSF levels of A , ubiquitin and total tau, and tau phosphorylated at various specific sites using the assays developed in Aim #1 in AD and control cases, and identify subgroups of AD based on these data by cluster analysis. APOE genotype frequencies and clinical profiles of each cluster, including symptoms such as depression, hallucinations, hypokinesia, and rigidity, will be analyzed. The % sensitivity and % specificity of each phosphorylation site at appropriate cut-off points will be determined to evaluate its diagnostic potential. (3) To study the relationship of levels of soluble and aggregated A 1, 2, ubiquitin and various phosphotaus between CSF and brain in Alzheimer's disease. Levels of soluble and aggregated A 2, ubiquitin and various phosphotaus will be assayed by ELISA and radioimmuno-dot-blots in the frozen autopsied brains of AD cases from which lumbar CSFs are available. The levels of these markers in the brain will be correlated to the histopathological staging of the disease, and to the CSF levels of these markers. These studies will help (i) identify subgroups of AD based on CSF markers, (ii) provide a lead on the nature of signaling pathways involved in various subgroups, (iii) reveal the diagnostic potential of CSF levels of tau phosphorylated at different specific sites and (iv) identify the relationship of the CSF levels of A , ubiquitin and tau to these markers in the brain and to the various histopathological stages of Alzheimer's disease. Better classification of AD at the molecular level and identification of biomarkers that represent the underlying disease process of various subtypes of the disease, in the long term, will lead to improved diagnosis and better defined treatment opportunities for AD and other tauopathies.
17 Resulting Publications
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1.
2013Jian-Zhi Wang; Yi-Yuan Xia; Inge Grundke-Iqbal; Khalid Iqbal
Journal of Alzheimer's disease : JAD 2013;33 Suppl 1():S123-39. -
2.
2011Khalid Iqbal; Inge Grundke-Iqbal
Opportunities and challenges in developing Alzheimer disease therapeutics.
Acta neuropathologica 2011;122(5):543-9. -
3.
2011Sonia Chalbot; Henrik Zetterberg; Kaj Blennow; Tormod Fladby; Niels Andreasen; Inge Grundke-Iqbal; Khalid Iqbal
Blood-cerebrospinal fluid barrier permeability in Alzheimer's disease.
Journal of Alzheimer's disease : JAD 2011;25(3):505-15. -
4.
2010K Iqbal; F Liu; C-X Gong; I Grundke-Iqbal
Tau in Alzheimer disease and related tauopathies.
Current Alzheimer research 2010;7(8):656-64. -
5.
2010Alejandra D Alonso; John Di Clerico; Bin Li; Christopher P Corbo; Maria E Alaniz; Inge Grundke-Iqbal; Khalid Iqbal
Phosphorylation of tau at Thr212, Thr231, and Ser262 combined causes neurodegeneration.
The Journal of biological chemistry 2010;285(40):30851-60. -
6.
2010Khalid Iqbal; Inge Grundke-Iqbal
Alzheimer's disease, a multifactorial disorder seeking multitherapies.
Alzheimer's & dementia : the journal of the Alzheimer's Association 2010;6(5):420-4. -
7.
2010Khalid Iqbal; Xiaochuan Wang; Julie Blanchard; Fei Liu; Cheng-Xin Gong; Inge Grundke-Iqbal
Alzheimer's disease neurofibrillary degeneration: pivotal and multifactorial.
Biochemical Society transactions 2010;38(4):962-6. -
8.
2010Sonia Chalbot; Henrik Zetterberg; Kaj Blennow; Tormod Fladby; Inge Grundke-Iqbal; Khalid Iqbal
Neuroscience letters 2010;478(3):179-83. -
9.
2010Norbert Zilka; Miroslava Korenova; Branislav Kovacech; Khalid Iqbal; Michal Novak
Acta neuropathologica 2010;119(6):679-87. -
10.
2009Sonia Chalbot; Henrik Zetterberg; Kaj Blennow; Tormod Fladby; Inge Grundke-Iqbal; Khalid Iqbal
Clinical chemistry 2009;55(12):2171-9. -
11.
2009Khalid Iqbal; Fei Liu; Cheng-Xin Gong; Alejandra Del C Alonso; Inge Grundke-Iqbal
Mechanisms of tau-induced neurodegeneration.
Acta neuropathologica 2009;118(1):53-69. -
12.
2009Hitoshi Tanimukai; Takashi Kudo; Toshihisa Tanaka; Inge Grundke-Iqbal; Khalid Iqbal; Masatoshi Takeda
Novel therapeutic strategies for neurodegenerative disease.
Psychogeriatrics : the official journal of the Japanese Psychogeriatric Society 2009;9(2):103-9. -
13.
2008Khalid Iqbal; M Omar Chohan; Inge Grundke-Iqbal
Journal of Alzheimer's disease : JAD 2008;15(2):339-45. -
14.
2008Khalid Iqbal; Alejandra del C Alonso; Inge Grundke-Iqbal
Journal of Alzheimer's disease : JAD 2008;14(4):365-70. -
15.
2008K Iqbal; I Grundke-Iqbal
Alzheimer neurofibrillary degeneration: significance, etiopathogenesis, therapeutics and prevention.
Journal of cellular and molecular medicine 2008;12(1):38-55. -
16.
2007K Iqbal; I Grundke-Iqbal
Developing pharmacological therapies for Alzheimer disease.
Cellular and molecular life sciences : CMLS 2007;64(17):2234-44. -
17.
2007Hidenaga Yamamori; Sabiha Khatoon; Inge Grundke-Iqbal; Kaj Blennow; Michael Ewers; Harald Hampel; Khalid Iqbal
Neuroscience letters 2007;418(2):186-9.
Scientific Context
This section shows information that has been computed by using the fingerprint of the grant, including related publications, related experts and related grants - all with fingerprints representing significant amounts of overlap between their fingerprint and this grant. The red dots indicate whether those experts or terms actually appear within this grant, showing potential and actual connections.
Related Grants
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1.
LEE, VIRGINIA M
Frontotemporal Dementias: Genotypes and Phenotypes
15 March 2000 - 29 February 2016
NATIONAL INSTITUTE ON AGING
Total Funding: $ 21,445,858
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2.
IQBAL, KHALID
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FOGARTY INTERNATIONAL CENTER
Total Funding: $ 70,352
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3.
IQBAL, KHALID
Abnormal Hyperphosphorylation of Tau
1 February 2001 - 30 April 2012
NATIONAL INSTITUTE ON AGING
Total Funding: $ 3,687,819
Related Publications
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1.
2003Takashi Horiguchi; Kunihiro Uryu; Benoit I Giasson; Harry Ischiropoulos; Richard LightFoot; Christine Bellmann; Christiane Richter-Landsberg; Virginia M-Y Lee; John Q Trojanowski
Nitration of tau protein is linked to neurodegeneration in tauopathies.
The American journal of pathology 2003;163(3):1021-31. -
2.
2004Antonella Vitali; Alessandra Piccini; Roberta Borghi; Pantaleo Fornaro; Sandra L Siedlak; Mark A Smith; Pierluigi Gambetti; Bernardino Ghetti; Massimo Tabaton
Soluble amyloid beta-protein is increased in frontotemporal dementia with tau gene mutations.
Journal of Alzheimer's disease : JAD 2004;6(1):45-51. -
3.
2002Luc Buée; Malika Hamdane; Patrice Delobel; Anne-Véronique Sambo; Séverine Bégard; Antoine Ghestem; Nicolas Sergeant; André Delacourte
[Tau story: from frontotemporal dementia to other tauopathies].
Journal de la Société de biologie 2002;196(1):103-8.
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