REVIEW: tau protein pathology in Alzheimer’s disease and related disorders

Neuropathology and Applied Neurobiology - Tập 25 Số 3 - Trang 171-187 - 1999
Markus Tolnay1, V PROBST1
1Institute of Pathology, Division of Neuropathology, Basel University, Basel, Switzerland,

Tóm tắt

Abundant neurofibrillary lesions made of hyperphosphorylated microtubule‐associated protein tau constitute one of the defining neuropathological features of Alzheimer’s disease. However, tau containing filamentous inclusions in neurones and/or glial cells also define a number of other neurodegenerative disorders clinically characterized by dementia and/or motor syndromes. All these disorders, therefore, are grouped under the generic term of tauopathies. In the first part of this review we outline the morphological and biochemical features of some major tauopathies, e.g. Alzheimer’s disease, argyrophilic grain disease, Pick’s disease, progressive supranuclear palsy and corticobasal degeneration. The impact of the recent finding of tau gene mutations in familial frontotemporal dementia and parkinsonism linked to chromosome 17 on other tauopathies is discussed in the second part. The review closes with a look towards a new understanding of neurodegenerative disorders characterized by filamentous nerve cell inclusions. The recent identification of the major protein component of their respective inclusions led to a surprising convergence of seemingly unrelated disorders. The new findings now allow us to classify neurodegenerative disorders with filamentous nerve cell inclusions into four main categories: (i) the tauopathies; (ii) the α‐synucleinopathies; (iii) the polyglutamine disorders; and (iv) the iquitin disorders’. Within the proposed classification scheme, tauopathies constitute the most frequent type of disorder.

Từ khóa


Tài liệu tham khảo

10.1021/bi00158a027

Askanas V, 1994, Twisted tubulofilaments of inclusion body myositis muscle resemble paired helical filaments of Alzheimer brain and contain hyperphosphorylated tau., Am J Pathol, 144, 177

Auer IA, 1995, Paired helical filament tau in Niemann‐Pick disease type C is similar to PHF‐tau in Alzheimer’s disease., Acta Neuropathol, 90, 547, 10.1007/BF00318566

10.1016/0006-8993(89)91396-6

10.1111/j.1750-3639.1998.tb00159.x

10.1016/0197-4580(89)90007-9

10.1007/s004010051077

Braak E, 1994, A sequence of cytoskeleton changes related to the formation of neurofibrillary tangles and neuropil threads., Acta Neuropathol, 87, 554, 10.1007/BF00293315

10.1016/0304-3940(87)90204-7

10.1111/j.1365-2990.1989.tb01146.x

10.1007/BF00308809

10.1016/S0002-9440(10)65272-8

10.1136/jnnp.57.4.416

Buée‐Scherrer V, 1995, Neurofibrillary degeneration in amyotrophic lateral sclerosis/parkinsonism‐dementia complex of Guam: immunochemical characterization of tau proteins., Am J Pathol, 146, 924

10.1002/ana.410420312

10.1097/00005072-199605000-00001

10.1002/ana.410410222

10.1016/S0140-6736(97)08360-8

10.1097/00005072-199602000-00004

10.1002/ana.410430209

10.1111/j.1750-3639.1998.tb00158.x

10.1097/00005072-199704000-00001

10.1016/0197-4580(92)90027-U

10.1093/brain/110.4.993

Feany MB, 1995, Widespread cytoskeletal pathology characterizes corticobasal degeneration., Am J Pathol, 146, 1388

10.1007/BF00294457

10.1097/00005072-199601000-00006

10.1016/0006-8993(90)90891-E

10.1007/BF00296367

10.1002/ana.410410606

Gallyas F, 1971, Silver staining of Alzheimer’s neurofibrillary changes by means of physical development., Acta Morph Acad Sci Hung, 19, 1

10.1111/j.1365-2990.1996.tb00840.x

10.1007/s004010050886

10.1073/pnas.93.2.744

10.1212/WNL.39.11.1453

10.1016/0304-3940(89)90169-9

10.1016/S0014-5793(97)00483-3

10.1038/383550a0

10.1016/0304-3940(95)11484-E

10.1016/0896-6273(92)90117-V

10.1016/S0959-4388(98)80090-1

10.1016/0896-6273(89)90210-9

GoedertM TrojanowskiJQ LeeVM‐YThe neurofibrillary pathology of Alzheimer’s disease. InThe Molecular and Genetic Basis of Neurological Diseases.Rosenberg RN Prusiner SB DiMauro S Barchi RL eds. Boston: Butterworth‐Heinemann 1997;61327

10.1002/j.1460-2075.1995.tb07116.x

10.1073/pnas.87.15.5827

Greenberg SG, 1992, Hydrofluoric acid‐treated tau PHF proteins display the same biochemical properties as normal tau., J Biol Chem, 267, 564, 10.1016/S0021-9258(18)48531-6

10.1016/S0166-2236(96)01030-2

10.1038/1565

10.1126/science.282.5391.1075

Hasegawa M, 1992, Protein sequence and mass spectrometric analyses of tau in the Alzheimer’s disease brain., J Biol Chem, 267, 7047, 10.1016/S0021-9258(18)41890-X

10.1074/jbc.272.52.33118

10.1016/S0014-5793(98)01217-4

10.1007/s004010050933

10.1212/WNL.50.1.270

10.1007/BF00294466

10.1126/science.282.5395.1914

10.1016/0006-8993(91)91467-F

10.1038/31508

10.1016/S0197-4580(98)00034-7

10.1007/BF00307644

10.1007/BF00318575

10.1046/j.1365-2990.1998.00108.x

10.1007/s004010050403

10.1111/j.1750-3639.1998.tb00160.x

10.1007/BF00334500

10.1007/BF00310916

10.1007/s004010050911

10.1136/jnnp.57.5.594

Ksiezak‐Reding H, 1994, Ultrastructure and biochemical composition of paired helical filaments in corticobasal degeneration., Am J Pathol, 149, 639

10.1016/0959-4388(95)80073-5

10.1126/science.1899488

10.1016/S0002-9440(10)65722-7

10.1097/00019052-199708000-00011

10.1093/brain/118.1.119

10.1016/S0014-5793(98)00910-7

10.1007/BF00294649

10.1074/jbc.270.2.823

10.1016/S0304-3940(97)00161-4

10.1001/archneur.55.8.1122

10.1046/j.1471-4159.1996.67031183.x

10.1002/ana.410430617

10.1016/0197-4580(91)90006-6

10.1111/j.1750-3639.1991.tb00666.x

10.1007/BF00688244

Probst A, 1993, Pathology of the striatum in progressive supranuclear palsy: abnormal tau proteins in astrocytes and cholinergic interneurons., Neurodegeneration, 2, 183

10.1007/s004010050565

10.1111/j.1750-3639.1998.tb00171.x

10.1097/00005072-199806000-00006

10.1136/jnnp.53.5.373

10.1016/S0197-4580(98)00022-0

10.1212/WNL.48.4.959

10.1111/j.1749-6632.1996.tb34401.x

10.1111/j.1750-3639.1998.tb00162.x

10.1007/s004010050487

10.1016/S0002-9440(10)65721-5

10.1016/S0166-2236(98)01337-X

10.1073/pnas.94.8.4113

10.1073/pnas.95.13.7737

10.1007/s004010051034

10.1046/j.1365-2990.1999.00164.x

10.1016/0006-8993(93)90226-D

10.1007/BF00703207

10.1097/00001756-199708180-00029

Tolnay M, 1999, Low amyloid (Aβ) plaque load and relative predominance of diffuse plaques distinguish argyrophilic grain disease from Alzheimer’s disease Neuropath Appl Neurobiol, 25

10.1046/j.1365-2990.1998.00090.x

10.1016/S0304-3940(98)00250-X

10.1007/s004010050887

10.1007/s004010050718

Tolnay M, 1999, Widespread tau pathology in hereditary frontotemporal dementia and parkinsonism: family SOT 254 (abstract)., Neuropathol Appl Neurobiol, 25, 146

10.1007/s004010050642

10.1212/WNL.47.3.711

Thông tin
Thông tin xuất bản

Neuropathology and Applied Neurobiology

Tập 25 Số 3

171-187

Thông tin tác giả