Tau protein abnormalities associated with the progression of alzheimer disease type dementia

被引:60
|
作者
Haroutunian, V.
Davies, P.
Vianna, C.
Buxbaum, J. D.
Purohit, D. P.
机构
[1] Vet Adm Med Ctr, Dept Psychiat, Bronx, NY 10468 USA
[2] Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA
[3] Albert Einstein Coll Med, Dept Pathol & Neurosci, Bronx, NY 10461 USA
[4] Mt Sinai Sch Med, Dept Pathol, New York, NY 10029 USA
关键词
Alzheimer disease; neurofibrillary tangles; tau; dementia; PAIRED HELICAL FILAMENTS; MILD COGNITIVE IMPAIRMENT; PREFRONTAL CORTEX AREA-9; NEUROFIBRILLARY TANGLES; REGIONAL-DISTRIBUTION; STEREOLOGIC ANALYSIS; BILATERAL SYMMETRY; NEURITIC PLAQUES; OLD PEOPLE; PATHOLOGY;
D O I
10.1016/j.neurobiolaging.2005.11.001
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
The degree to which neurofibrillary tangles (NIFT), the hallmark lesions of Alzheimer disease (AD), contribute to the development of the cognitive symptoms of AD has been debated. NFTs are comprised of abnormally phosphorylated and conformationally altered tau proteins. Conformational changes in tau have been proposed to be among the earliest neurobiological changes in AD. This study examined whether conformational changes detected by antibodies MCl and TG3 represent early abnormalities in the disease process by assessing their presence at different stages of dementia in multiple brain regions. Postmortem specimens from several neocortical regions were examined for conformational changes in tau by ELISA in subjects [n = 81] who died at different stages of cognitive impairment. Concentrations of conformationally altered tau increased with increasing dementia severity and the levels of MCl immunoreactivity increased in the frontal cortex of mildly demented subjects before the appearance of NFT bearing neurons, suggesting that conformational alterations in tau occur early in the course of AD and its cognitive symptoms and may precede histologically identified NFTs. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:1 / 7
页数:7
相关论文
共 50 条
  • [31] Targeting Tau Protein in Alzheimer's Disease
    Gong, Cheng-Xin
    Grundke-Iqbal, Inge
    Iqbal, Khalid
    DRUGS & AGING, 2010, 27 (05) : 351 - 365
  • [32] Targeting tau protein in Alzheimer's disease
    Rafii, Michael S.
    LANCET, 2016, 388 (10062): : 2842 - 2844
  • [33] Tau polymorphisms are not associated with Alzheimer's disease
    Kwon, JM
    Nowotny, P
    Shah, PK
    Chakraverty, S
    Norton, J
    Morris, JC
    Goate, AM
    NEUROSCIENCE LETTERS, 2000, 284 (1-2) : 77 - 80
  • [34] Tracking of Alzheimer's disease progression with cerebrospinal fluid tau protein phosphorylated at threonine 231
    Hampel, H
    Buerger, K
    Kohnken, R
    Teipel, SJ
    Zinkowski, R
    Moeller, HJ
    Rapoport, SI
    Davies, P
    ANNALS OF NEUROLOGY, 2001, 49 (04) : 545 - 546
  • [35] EFFECT OF SEIZURES ON PROGRESSION OF DEMENTIA OF THE ALZHEIMER-TYPE
    VOLICER, L
    SMITH, S
    VOLICER, BJ
    DEMENTIA, 1995, 6 (05): : 258 - 263
  • [36] ACCELERATED PROGRESSION OF DEMENTIA OF THE ALZHEIMER TYPE BY DEVELOPMENT OF SEIZURES
    VOLICER, L
    SMITH, S
    NEUROBIOLOGY OF AGING, 1990, 11 (03) : 255 - 255
  • [37] Regional Cerebral Blood Flow Abnormalities Associated with Apathy and Depression in Dementia of the Alzheimer's Type
    Kang, J.
    Lee, J.
    Kang, H.
    Lee, H.
    Kim, Y.
    Jeon, H.
    Chung, J.
    Lee, M.
    Cho, M.
    Lee, D.
    EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING, 2010, 37 : S260 - S260
  • [38] Progression of Tau and neuroinflammation PET are independently associated with structural network reorganization in Alzheimer's disease
    Ottoy, Julie
    Kang, Min-Su
    Isen, Jonah
    Bezgin, Gleb
    Soucy, Jean-Paul
    Gauthier, Serge
    Black, Sandra E.
    Rosa-Neto, Pedro
    Goubran, Maged
    JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2021, 41 (1_SUPPL): : 173 - 174
  • [39] Cerebrospinal fluid cortisol and clinical disease progression in MCI and dementia of Alzheimer's type
    Popp, Julius
    Wolfsgruber, Steffen
    Heuser, Isabella
    Peters, Oliver
    Huell, Michael
    Schroeder, Johannes
    Moeller, Hans-Juergen
    Lewczuk, Piotr
    Schneider, Anja
    Jahn, Holger
    Luckhaus, Christian
    Perneczky, Robert
    Froelich, Lutz
    Wagner, Michael
    Maier, Wolfgang
    Wiltfang, Jens
    Kornhuber, Johannes
    Jessen, Frank
    NEUROBIOLOGY OF AGING, 2015, 36 (02) : 601 - 607