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Tauopathy

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For the alternative medicine practice similar to homeopathy, see tautopathy.
Tauopathy
SpecialtyNeurology Edit this on Wikidata
Diagram of a normal microtubule and one affected by tauopathy

Tauopathy belongs to a class of neurodegenerative diseases associated with the pathological aggregation of tau protein in neurofibrillary or gliofibrillary tangles[1] in the human brain. Tangles are formed by hyperphosphorylation of a microtubule-associated protein known as tau, causing it to aggregate in an insoluble form. (These aggregations of hyperphosphorylated tau protein are also referred to as paired helical filaments). The precise mechanism of tangle formation is not completely understood, and it is still controversial as to whether tangles are a primary causative factor in the disease or play a more peripheral role. Primary tauopathies, i.e., conditions in which neurofibrillary tangles (NFT) are predominantly observed, include:

Neurofibrillary tangles were first described by Alois Alzheimer in one of his patients suffering from Alzheimer's disease (AD), which is considered a secondary tauopathy. AD is also classified as an amyloidosis because of the presence of senile plaques.[2]

The degree of NFT involvement in AD is defined by Braak stages. Braak stages I and II are used when NFT involvement is confined mainly to the transentorhinal region of the brain, stages III and IV when there's also involvement of limbic regions such as the hippocampus, and V and VI when there's extensive neocortical involvement. This should not be confused with the degree of senile plaque involvement, which progresses differently.[14]

In both Pick's disease and corticobasal degeneration, tau proteins are deposited as inclusion bodies within swollen or "ballooned" neurons.[15]

Argyrophilic grain disease (AGD), another type of dementia,[16][17][18] is marked by an abundance of argyrophilic grains and coiled bodies upon microscopic examination of brain tissue.[19] Some consider it to be a type of Alzheimer's disease.[19] It may co-exist with other tauopathies such as progressive supranuclear palsy and corticobasal degeneration,[2] and also Pick's disease.[20]

Huntington's disease (HD): a neurodegenerative disease caused by a CAG tripled expansion in the Huntington gene is the most recently described tauopathy (Fernandez-Nogales et al. Nat Med 2014). JJ Lucas and co-workers demonstrate that, in brains with HD, tau levels are increased and the 4R/3R balance is altered. In addition, the Lucas study shows intranuclear insoluble deposits of tau; these "Lucas' rods" were also found in brains with Alzheimer's disease.

Tauopathies are often overlapped with synucleinopathies, possibly due to interaction between the synuclein and tau proteins.[21][22]

The non-Alzheimer's tauopathies are sometimes grouped together as "Pick's complex" due to their association with frontotemporal dementia, or frontotemporal lobar degeneration.[23][24][25]

See also

References

  1. ^ Rizzo, G.; Martinelli, P.; Manners, D.; Scaglione, C.; Tonon, C.; Cortelli, P.; Malucelli, E.; Capellari, S.; et al. (2008). "Diffusion-weighted brain imaging study of patients with clinical diagnosis of corticobasal degeneration, progressive supranuclear palsy and Parkinson's disease". Brain. 131 (Pt 10): 2690–700. doi:10.1093/brain/awn195. PMID 18819991.
  2. ^ a b c Dickson, DW (2009). "Neuropathology of Non-Alzheimer Degenerative Disorders". International Journal of Clinical and Experimental Pathology. 3 (1): 1–23. PMC 2776269. PMID 19918325.
  3. ^ Santa-Maria, Ismael; Haggiagi A; Liu X; Wasserscheid J; Nelson PT; Dewar K; Clark LN; Crary JF (Nov 2012). "The MAPT H1 haplotype is associated with tangle-predominant dementia". Acta Neuropathologica. 124 (5): 693–704. doi:10.1007/s00401-012-1017-1. PMC 3608475. PMID 22802095.
  4. ^ Jellinger, K. A.; Attems, J. (2006). "Neurofibrillary tangle-predominant dementia: comparison with classical Alzheimer disease". Acta Neuropathologica. 113 (2): 107–17. doi:10.1007/s00401-006-0156-7. PMID 17089134.
  5. ^ Mckee, Ann C.; Cairns, Nigel J. (2016). "The first NINDS/NIBIB consensus meeting to define neuropathological criteria for the diagnosis of chronic traumatic encephalopathy". Acta Neuropathologica. 131 (1): 75–86. doi:10.1007/s00401-015-1515-z. PMC 4698281. PMID 26667418.
  6. ^ Roberts, GW (1988). "Immunocytochemistry of neurofibrillary tangles in dementia pugilistica and Alzheimer's disease: evidence for common genesis". Lancet. 2 (8626–8627): 1456–58. doi:10.1016/S0140-6736(88)90934-8. PMID 2904573.
  7. ^ Williams, David R; Lees, Andrew J (2009). "Progressive supranuclear palsy: clinicopathological concepts and diagnostic challenges". The Lancet Neurology. 8 (3): 270–79. doi:10.1016/S1474-4422(09)70042-0. PMID 19233037.
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  9. ^ Hof, P. R.; Nimchinsky, E. A.; Buée-Scherrer, V.; Buée, L.; Nasrallah, J.; Hottinger, A. F.; Purohit, D. P.; Loerzel, A. J.; et al. (1994). "Amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam: quantitative neuropathology, immunohistochemical analysis of neuronal vulnerability, and comparison with related neurodegenerative disorders". Acta Neuropathologica. 88 (5): 397–404. doi:10.1007/BF00389490. PMID 7847067.
  10. ^ Brat, Daniel J.; Gearing, Marla; Goldthwaite, Patricia T.; Wainer, Bruce H.; Burger, Peter C. (2001). "Tau-associated neuropathology in ganglion cell tumours increases with patient age but appears unrelated to ApoE genotype". Neuropathology and Applied Neurobiology. 27 (3): 197–205. doi:10.1046/j.1365-2990.2001.00311.x. PMID 11489139.
  11. ^ Halper, J; Scheithauer, BW; Okazaki, H; Laws Jr, ER (1986). "Meningio-angiomatosis: a report of six cases with special reference to the occurrence of neurofibrillary tangles". Journal of neuropathology and experimental neurology. 45 (4): 426–46. doi:10.1097/00005072-198607000-00005. PMID 3088216.
  12. ^ Paula-Barbosa, M. M.; Brito, R.; Silva, C. A.; Faria, R.; Cruz, C. (1979). "Neurofibrillary changes in the cerebral cortex of a patient with subacute sclerosing panencephalitis (SSPE)". Acta Neuropathologica. 48 (2): 157–60. doi:10.1007/BF00691159. PMID 506699.
  13. ^ Wisniewski, Krystyna; Jervis, George A.; Moretz, Roger C.; Wisniewski, Henryk M. (1979). "Alzheimer neurofibrillary tangles in diseases other than senile and presenile dementia". Annals of Neurology. 5 (3): 288–94. doi:10.1002/ana.410050311. PMID 156000.
  14. ^ Braak, H.; Braak, E. (1991). "Neuropathological stageing of Alzheimer-related changes". Acta Neuropathologica. 82 (4): 239–59. doi:10.1007/BF00308809. PMID 1759558.
  15. ^ Arai, Tetsuaki; Ikeda, Kenji; Akiyama, Haruhiko; Shikamoto, Yasuo; Tsuchiya, Kuniaki; Yagishita, Saburo; Beach, Thomas; Rogers, Joseph; et al. (2001). "Distinct isoforms of tau aggregated in neurons and glial cells in brains of patients with Pick's disease, corticobasal degeneration and progressive supranuclear palsy". Acta Neuropathologica. 101 (2): 167–73. doi:10.1007/s004010000283 (inactive 2017-01-15). PMID 11271372.{{cite journal}}: CS1 maint: DOI inactive as of January 2017 (link)
  16. ^ Ferrer I, Santpere G, van Leeuwen FW (2008). "Argyrophilic grain disease". Brain. 131 (Pt 6): 1416–32. doi:10.1093/brain/awm305. PMID 18234698.
  17. ^ Josephs KA, Whitwell JL, Parisi JE, Knopman DS, Boeve BF, Geda YE, Jack CR Jr, Petersen RC, Dickson DW (2008). "Argyrophilic grains: a distinct disease or an additive pathology?". Neurobiology of Aging. 29 (4): 566–73. doi:10.1016/j.neurobiolaging.2006.10.032. PMC 2727715. PMID 17188783.
  18. ^ Wallon, D.; Sommervogel, C.; Laquerrière, A.; Martinaud, O.; Lecourtois, M.; Hannequin, D. (2010). "Maladie des grains argyrophiles : composante synergique de la démence ?" [Argyrophilic grain disease: synergistic component of dementia?]. Revue neurologique (in French). 166 (4): 428–32. doi:10.1016/j.neurol.2009.10.012. PMID 19963233.
  19. ^ a b Tolnay, M; Monsch, AU; Staehelin, HB; Probst, A (1999). "Argyrophilic grain disease: differentiation from Alzheimer disease". Der Pathologe. 20 (3): 159–68. PMID 10412175.
  20. ^ Jellinger KA (1998). "Dementia with grains (argyrophilic grain disease". Brain Pathology. 8 (2): 377–86. doi:10.1111/j.1750-3639.1998.tb00161.x. PMID 9546294.
  21. ^ Simon Moussaud; Daryl R Jones; Elisabeth L Moussaud-Lamodière; Marion Delenclos; Owen A Ross; Pamela J McLean (corresponding author) (October 2014). "Alpha-synuclein and tau: teammates in neurodegeneration?". Mol Neurodegener. 9: 43. doi:10.1186/1750-1326-9-43. PMC 4230508. PMID 25352339. {{cite journal}}: |author6= has generic name (help); Unknown parameter |last-author-amp= ignored (|name-list-style= suggested) (help)CS1 maint: unflagged free DOI (link)
  22. ^ Jing L. Guo; Dustin J. Covell; Joshua P. Daniels; Michiyo Iba; Anna Stieber; Bin Zhang; Dawn M. Riddle; Linda K. Kwong; Yan Xu; John Q. Trojanowski; Virginia M.Y. Lee (July 2013). "Distinct α-Synuclein Strains Differentially Promote Tau Inclusions in Neurons". Cell. 154 (1): 103–17. doi:10.1016/j.cell.2013.05.057. PMC 3820001. PMID 23827677. {{cite journal}}: Unknown parameter |last-author-amp= ignored (|name-list-style= suggested) (help)
  23. ^ Kertesz, Andrew (2003). "Pick Complex: An Integrative Approach to Frontotemporal Dementia". The Neurologist. 9 (6): 311–17. doi:10.1097/01.nrl.0000094943.84390.cf. PMID 14629785.
  24. ^ Kertesz, Andrew (2003). "Pick's complex and FTDP-17". Movement Disorders. 18: 57–62. doi:10.1002/mds.10564.
  25. ^ Andrew Kertesz; Paul McMonagle; Mervin Blair; Wilda Davidson; David G. Munoz (July 20, 2005). "The evolution and pathology of frontotemporal dementia". Brain. 128 (9): 1996–2005. doi:10.1093/brain/awh598. PMID 16033782.
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