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'''Filamen PH''' ({{lang-en|neurofibrillary tangle, paired helical filaments, PHF}}) adalah tumpukan [[protein]] yang ditemukan pertama kali oleh [[Alois Alzheimer]] di dalam [[neuron]] penderita [[Alzheimer]],.<ref>{{Cite pertamaweb|last=alzi|date=2019-06-15|title=Apa kaliyang olehmenyebabkan [[Alois Alzheimer]]demensia?|url=https://alzi.or.id/apa-yang-menyebabkan-demensia/|website=Alzheimer Indonesia|language=en|access-date=2024-09-28}}</ref>▼
[[Berkas:TAU_HIGH.JPG|thumb|right|150px|Protein Tau yang mengalami hiperfosforilasi menjadi filamen tak larut]]
▲'''Filamen PH''' ({{lang-en|neurofibrillary tangle, paired helical filaments, PHF}}) adalah tumpukan [[protein]] yang ditemukan di dalam [[neuron]] penderita [[Alzheimer]], pertama kali oleh [[Alois Alzheimer]].
 
Filamen ini terbentuk dari berbagai [[isomer]]<ref>{{en}} {{cite web
Filamen ini terbentuk karena [[protein tau]] - sebuah [[protein]] yang berperan dalam perakitan dan pemeliharaan struktur [[mikrotubula]] - mengalami [[hiperfosforilasi]] sehingga memecahkan struktur mikrotubula. Radikal protein tau, kemudian berhimpun menjadi filamen PH.<ref name="PM20553310">{{en}}{{cite web▼
| url = http://www.ncbi.nlm.nih.gov/pubmed/2484340
| title = Multiple isoforms of human microtubule-associated protein tau: sequences and localization in neurofibrillary tangles of Alzheimer's disease
| accessdate = 2010-06-27
| work = Medical Research Council, Laboratory of Molecular Biology, Cambridge, England; Goedert M, Spillantini MG, Jakes R, Rutherford D, Crowther RA.
| archive-date = 2019-12-15
| archive-url = https://web.archive.org/web/20191215025836/https://www.ncbi.nlm.nih.gov/pubmed/2484340
| dead-url = no
}}</ref> dan [[fosfotreonil protein fosfatasetau]].<ref>{{en}} {{cite web▼
| url = http://www.ncbi.nlm.nih.gov/pubmed/3131773
| title = Cloning and sequencing of the cDNA encoding a core protein of the paired helical filament of Alzheimer disease: identification as the microtubule-associated protein tau
| accessdate = 2010-06-27
| work = Medical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom; Goedert M, Wischik CM, Crowther RA, Walker JE, Klug A.
| archive-date = 2019-04-01
| archive-url = https://web.archive.org/web/20190401194515/https://www.ncbi.nlm.nih.gov/pubmed/3131773
| dead-url = no
▲Filamen ini terbentuk karena [[protein tau]]}}</ref> - sebuah [[protein]] yang berperan dalam perakitan dan pemeliharaan struktur [[mikrotubula]] - mengalami [[hiperfosforilasi]] sehingga memecahkan struktur [[mikrotubula]]. Radikal protein tau, kemudian berhimpun menjadi filamen PH di dalam [[soma]].<ref name="PM20553310">{{en}} {{cite web
| url = http://www.ncbi.nlm.nih.gov/pubmed/20553310
| title = The Role of Tau in Alzheimer's Disease and Related Disorders
| accessdate = 2010-06-21
| work = Department of Neurobiology and Behavior and Institute for Memory Impairments and Neurological Disorders, University of California; Medeiros R, Baglietto-Vargas D, Laferla FM.
| archive-date = 2019-12-25
| archive-url = https://web.archive.org/web/20191225004208/https://www.ncbi.nlm.nih.gov/pubmed/20553310
| dead-url = no
}}</ref>
 
Hiperfosforilasi terjadi karena terjadi kerusakan transduksi sinyal selularseluler yang disebabkan oleh tidaktid ak seimbangnya aktivitas [[protein]] dari beberapa [[enzim]] [[kinasefosfatase]] dan [[fosfatasekinase]].,<ref name="PM20553310" /> Prosesseperti kimiawi''calmodulin-dependent iniprotein dapatkinase diredam dengan meningkatkan aktivitasII'', ''[[enzimglycogen synthase kinase-3beta]]'' [[fosfoserildan ''cyclin-dependent protein fosfatase]]kinase 5''.<ref>{{en}} {{cite web
| url = http://www.ncbi.nlm.nih.gov/pubmed/18194444
| title = Alzheimer neurofibrillary degeneration: significance, etiopathogenesis, therapeutics and prevention
| accessdate = 2010-06-21
| work = Department of Neurochemistry New York State Institute for Basic Research in Developmental Disabilities; Iqbal K, Grundke-Iqbal I.
| archive-date = 2016-06-11
| archive-url = https://web.archive.org/web/20160611142209/http://www.ncbi.nlm.nih.gov/pubmed/18194444
| dead-url = no
}}</ref><ref>{{en}} {{cite web
| url = http://www.ncbi.nlm.nih.gov/pubmed/17241267
| title = Kinases and phosphatases and tau sites involved in Alzheimer neurofibrillary degeneration
| accessdate = 2010-06-21
| work = Pathophysiology Department, Tongji Medical College, Huazhong University of Science & Technology; Wang JZ, Grundke-Iqbal I, Iqbal K.
| archive-date = 2017-07-15
| archive-url = https://web.archive.org/web/20170715052648/https://www.ncbi.nlm.nih.gov/pubmed/17241267
| dead-url = no
}}</ref> Proses kimiawi ini dapat diredam dengan meningkatkan aktivitas [[enzim]] [[fosfoseril protein fosfatase]]<ref>{{en}} {{cite web
| url = http://www.ncbi.nlm.nih.gov/pubmed/15270196
| title = Inhibition of neurofibrillary degeneration: a promising approach to Alzheimer's disease and other tauopathies
| accessdate = 2010-06-21
| work = Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities; Iqbal K, Grundke-Iqbal I.
| archive-date = 2023-07-21
▲}}</ref> dan [[fosfotreonil protein fosfatase]].<ref>{{en}}{{cite web
| archive-url = https://web.archive.org/web/20230721053109/https://pubmed.ncbi.nlm.nih.gov/15270196/
| dead-url = no
}}</ref> dan [[fosfotreonil protein fosfatase]].<ref>{{en}} {{cite web
| url = http://www.ncbi.nlm.nih.gov/pubmed/10961432
| title = Mechanism of neurofibrillary degeneration and pharmacologic therapeutic approach
| accessdate = 2010-06-21
| work = New York State Institute for Basic Research in Developmental Disabilities; Iqbal K, Alonso AD, Gondal JA, Gong CX, Haque N, Khatoon S, Sengupta A, Wang JZ, Grundke-Iqbal I.
| archive-date = 2019-04-10
| archive-url = https://web.archive.org/web/20190410171022/https://www.ncbi.nlm.nih.gov/pubmed/10961432
| dead-url = no
}}</ref>
 
== Rujukan ==▼
 
Activities of phosphoseryl/phosphothreonyl protein phosphatases (PP)-2A and PP-1 which can dephosphorylate the abnormal tau to a normal-like state are compromised in AD brain. Dephosphorylation by PP-2A and PP-2B and to a lesser extent by PP-1 restores the normal microtubule assembly promoting activity in AD P-tau in vitro. Neurofibrillary tangles of PHF isolated from AD brain are also dissociated on in vitro dephosphorylation with PP-2A, and the tau released by this treatment can stimulate microtubule assembly. Thus, it appears that the abnormal hyperphosphorylation of tau leads to neurodegeneration through breakdown of the microtubule network and that the abnormal tau on association with normal tau forms neurofibrillary tangles of tau filaments i.e. PHF/SF. Increase in tau phosphatase activity is a promising approach to inhibit neurofibrillary degeneration and thereby the diseases characterized by this lesion.
 
 
▲==Rujukan==
{{reflist}}
 
[[Kategori:Biologi selProtein]]
 
[[en:Neurofibrillary tangle]]
[[es:Ovillo neurofibrilar]]
[[it:Ammassi neurofibrillari]]
[[pl:Splątki neurofibrylarne]]
[[ru:Нейрофибриллярный клубок]]
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