Proteina tau

Proteina tau MAPT
Alia nomina	MAPT, DDPAC, FTDP-17, MAPTL, MSTD, MTBT1, MTBT2, PPND, PPP1R103,
Locus geni (homo)

Chromosoma	17 (humanum)
Locus	17q21.31 (homo)

Fontes externae	OMIM: 157140

Proteina tau est proteina, quae forma cytosceleti neuronorum in parte determinatur^[1]. Noti sunt sex subtypi proteinarum tau.

In quibusdam morbis neurodegenerativis degeneratio proteinarum tau phosphorylatione observatur, quo fit, ut in dignoscendis morbis neurodegenerativis aestimatio valoris proteinea tau in liquore spinali momentum habeat.

Natura proteinae Tau

Forma cellularum, ut systematis nervosi centralis, imprimis matricibus intracellularibus, cytosceleto determinatur. Videtur hoc quoque in neuronibus, quo microtubuli principalia membra illius cytosceleti sunt. Ad structuram eius stabiliendam proteinae tau stabilitores pernecesse sunt.

Genetica

Nomen geni proteinae Tau est MAPT locus cuius geneticus in chromosomate 17 humano invenitur (17q21.31). Numerus aminoacidorum ab 352 ad 441 est.

Anatomia pathologica

In morbo cerebrorum Alzheimeriano aegrotis microscopiae ope aggregatae proteinarum tau fibrillae, neurofibrillae dictae, inveniuntur^[2].

Physiologia pathologica

Experimentum SCHALERi et al.: Stimulatio receptorii PAC1 reductionem proteinae tau postsynapticae in mure perficit. AC adenylati cyclasis, cAMP adenosinum triphosphatum cyclicum, PK A proteini kinasis A

In tauopathiis proteinam tau ex microtubulis dissolutis et in synapsum terminalium vicinate et in postsynapsem accumulat. Videtur, ut impromis accumulatio proteinae tau postsynaptica detrimentum systemati nervoso imponat. Nuper in laboratorio destructio proteinarum tau postsynapticorum ope peptida adenylati cyclasem activans pituitaria (PACAP) et receptorium eius (receptorium PAC 1) contigit^[3].

Res continentes morbis

Consocatio valores aucti proteinae tau in liquore cerebrospinali initium vel praesentiam morbi neurodegenerativi proponere queat, ut morbum Alzheimerianum.

Insomnia

Nuper divulgatum est valores auctos secundum insomniam observari posse; Conclusio quidem, ut insomia periculum dementiae augere possit, non valida esset^[4].

Notae

↑ Avila J., Lucas J. J., Perez M., Hernandez F. (2004). "Role of tau protein in both physiological and pathological conditions". Physiological reviews 84 (2): 361-84
↑ Chun W., Johnson G. V. (2007). "The role of tau phosphorylation and cleavage in neuronal cell death". Frontiers in bioscience 12: 733-56
↑ Schaler A. W., Runyan A. M., Clelland C. L., Sydney E. J., Fowler S. L., Figueroa H. Y., Shioda S., Santa-Maria I., Duff K. E., Myeku N. (Mai 2021). "PAC1 receptor-mediated clearance of tau in postsynaptic compartments attenuates tau pathology in mouse brain". Science translational medicine 13 (595): eaba7394
↑ Benedict C., Blennow K., Zetterberg H,, Cedernaes J. (Ian 2020). "Effects of acute sleep loss on diurnal plasma dynamics of CNS health biomarkers in young men". Neurology: 1212/WNL.0000000000008866

Nexus interni

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[1] Avila J., Lucas J. J., Perez M., Hernandez F. (2004). "Role of tau protein in both physiological and pathological conditions". Physiological reviews 84 (2): 361-84

[2] Chun W., Johnson G. V. (2007). "The role of tau phosphorylation and cleavage in neuronal cell death". Frontiers in bioscience 12: 733-56

[3] Schaler A. W., Runyan A. M., Clelland C. L., Sydney E. J., Fowler S. L., Figueroa H. Y., Shioda S., Santa-Maria I., Duff K. E., Myeku N. (Mai 2021). "PAC1 receptor-mediated clearance of tau in postsynaptic compartments attenuates tau pathology in mouse brain". Science translational medicine 13 (595): eaba7394

[4] Benedict C., Blennow K., Zetterberg H,, Cedernaes J. (Ian 2020). "Effects of acute sleep loss on diurnal plasma dynamics of CNS health biomarkers in young men". Neurology: 1212/WNL.0000000000008866

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