155:(no signs of dementia). One current hypothesis suggests that PART related dementia could be infrequent in younger populations, but may show symptomatic onset within oldest old (people greater than 90 years old). Given that the elderly represent a fast growing segment of the population worldwide, further research is needed to understand how PART related pathological process can manifest in specific clinical symptoms.
294:
arrangement. PART cases is due to tau protein isoforms (3 and 4 microtubule binding repeats) abnormal ration inneural cells resulting in their self assembling and accumulation resulting in NFT formation in brain. Detachment of tau from microtubules causes the neuron to lose its ability to sustain
354:
These options listed below have not been yet linked or specified for PART treatment since the disease is yet to gain acceptance as a unique abnormality case by the medical community. Thus the treatments represent possible future options as per the research and finding in the medical literature.
174:
Given the similarities in the pattern of neurofibrillary tangles in PART, some scientists have argued that they represent the same phenomenon. However, others have argued that sufficient evidence exists to conclude that PART represents a pathological process. Further more,
302:
but since PART cases generally lack senile plaques, other causes were investigated. One such cause was found to me the microtubule affinity-regulating kinase (MARK) since it is involved in tau phosphorylation and dephosphorylation.
228:. Transformation in tau gene on chromosome 17 can be linked to PART due to the fact that the tau protein analyzed from PART NFTs consist of 3R and 4R isoforms. MAPT gene results in different tau protein isoforms due to
187:
is absent in PART and due to several mechanisms underlying tau formation and maintenance, it would be necessary to separate PART from AD due to implications with respect to developing diagnostics and therapeutics.
608:
Jellinger, Kurt A.; Alafuzoff, Irina; Attems, Johannes; Beach, Thomas G.; Cairns, Nigel J.; Crary, John F.; Dickson, Dennis W.; Hof, Patrick R.; Hyman, Bradley T.; Jack, Clifford R.; Jicha, Gregory A. (May 2015).
550:
Duyckaerts, Charles; Braak, Heiko; Brion, Jean-Pierre; Buée, Luc; Del
Tredici, Kelly; Goedert, Michel; Halliday, Glenda; Neumann, Manuela; Spillantini, Maria Grazia; Tolnay, Markus; Uchihara, Toshiki (May 2015).
1320:
Lasagna-Reeves, Cristian A.; Castillo-Carranza, Diana L.; Guerrero-Muñoz, Marcos J.; Jackson, George R.; Kayed, Rakez (2010-11-30). "Preparation and
Characterization of Neurotoxic Tau Oligomers".
737:
Josephs, Keith A.; Murray, Melissa E.; Tosakulwong, Nirubol; Whitwell, Jennifer L.; Knopman, David S.; Machulda, Mary M.; Weigand, Stephen D.; Boeve, Bradley F.; Kantarci, Kejal (2017-02-03).
147:. Braak state 0 is restricted to the cortex, state l-ll bound by transentorhinal region and it can progress into limbic region of the brain (stage lll-lV). PART can be further categorized as
271:
Owing to these imaging and staining advancements, tau has been identified to be associated with microtubules in neuron cells. Tau protein stabilize the microtubules and are involved in fast
290:) and microtubule binding domain. Tau in brain of patients with tauopathies is hyperphosphorylated which causes the tau protein to dissociate from the microtubule then aggregate in to
216:
strongly linked to AD. Thus another piece of evidence supporting the hypothesis that PART represents a novel diagnostic category. Also transformation as a result of tau mutation into
493:
Crary, John F.; Trojanowski, John Q.; Schneider, Julie A.; Abisambra, Jose F.; Abner, Erin L.; Alafuzoff, Irina; Arnold, Steven E.; Attems, Johannes; Beach, Thomas G. (2014-12-01).
436:
Crary, John F.; Trojanowski, John Q.; Schneider, Julie A.; Abisambra, Jose F.; Abner, Erin L.; Alafuzoff, Irina; Arnold, Steven E.; Attems, Johannes; Beach, Thomas G. (2014-12-01).
1146:
Duyckaerts, Charles; Braak, Heiko; Brion, Jean-Pierre; Buée, Luc; Del
Tredici, Kelly; Goedert, Michel; Halliday, Glenda; Neumann, Manuela; Spillantini, Maria Grazia (2015-05-01).
1586:
Santa-Maria, Ismael; Alaniz, Maria E.; Renwick, Neil; Cela, Carolina; Fulga, Tudor A.; Vactor, David Van; Tuschl, Thomas; Clark, Lorraine N.; Shelanski, Michael L. (2015-02-02).
1203:
Jellinger, Kurt A.; Alafuzoff, Irina; Attems, Johannes; Beach, Thomas G.; Cairns, Nigel J.; Crary, John F.; Dickson, Dennis W.; Hof, Patrick R.; Hyman, Bradley T. (2015-05-01).
739:"Tau aggregation influences cognition and hippocampal atrophy in the absence of beta-amyloid: a clinico-imaging-pathological study of primary age-related tauopathy (PART)"
52:
1095:
Braak, Heiko; Del
Tredici, Kelly (2014-12-01). "Are cases with tau pathology occurring in the absence of Aβ deposits part of the AD-related pathological process?".
252:
tools have allowed researchers to identify and observe tau protein aggregation both intra and intercellullary as well as their interaction with other proteins.
135:. Specifically, higher stages of tangle burden (i.e. Braak III or IV) in PART have been found to be associated with more rapid decline on tasks involving
797:
Santa-Maria, Ismael; Haggiagi, Aya; Liu, Xinmin; Wasserscheid, Jessica; Nelson, Peter T.; Dewar, Ken; Clark, Lorraine N.; Crary, John F. (2012-11-01).
51:). Despite some controversy, the term PART has been widely adopted, with the consensus criteria cited over 1130 times as of April 2023 according to
43:(AD). The term and diagnostic criteria for PART were developed by a large group of neuropathologists, spearheaded by Drs. John F. Crary (then at
919:
Saint-Aubert, Laure; Lemoine, Laetitia; Chiotis, Konstantinos; Leuzy, Antoine; Rodriguez-Vieitez, Elena; Nordberg, Agneta (20 February 2017).
315:
and MARK hyper-phosphorylate the mutant tau protein residue. Also researcher have linked to NFT survive (mutant tau protein maintenance) to
1378:
Luo, Wenjie; Dou, Fei; Rodina, Anna; Chip, Sophorn; Kim, Joungnam; Zhao, Qi; Moulick, Kamalika; Aguirre, Julia; Wu, Nian (2007-05-29).
390:
and inhibit MARK which consequently down regulation tau protein hyper-phosphorylation and ultimately its detachment from microtubules.
44:
339:
265:
58:
At autopsy, the hallmark of PART is the presence of
Alzheimer-type neurofibrillary tangles (NFTs) composed of abnormal
163:
307:
of MARK gene results in excessive tau phosphorylation and eventually NFT's formation. It is suspected that at a
86:
cases have been shown to display this pattern of degeneration. Patients with severe PART typically exhibit mild
1380:"Roles of heat-shock protein 90 in maintaining and facilitating the neurodegenerative phenotype in tauopathies"
383:
387:
225:
28:
1524:
Moszczynski, Alexander J.; Yang, Wencheng; Hammond, Robert; Ang, Lee Cyn; Strong, Michael J. (2017-01-11).
111:
that are essentially identical to those occurring in mild to moderate-stage
Alzheimer's disease and other
108:
48:
40:
1588:"Dysregulation of microRNA-219 promotes neurodegeneration through post-transcriptional regulation of tau"
1454:
Annadurai, Narendran; Agrawal, Khushboo; Džubák, Petr; Hajdúch, Marián; Das, Viswanath (November 2017).
408:
221:
1526:"Threonine175, a novel pathological phosphorylation site on tau protein linked to multiple tauopathies"
268:(PET) imaging allowing for both intracellular and extracellular observation of tau protein behaviours.
123:
are found, Thal phase grading can be implemented to differentiate the pathology as either PART or AD.
1391:
343:
253:
180:
87:
82:. 18% of Alzheimer neuropathological changes in cognitively normal and 5% of cognitively impaired
1501:
1456:"Microtubule affinity-regulating kinases are potential druggable targets for Alzheimer's disease"
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since in fly model brain, over expression of miRNA-219 reduced the tau protein accumulation.
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Jefferson-George, Kyra S.; Wolk, David A.; Lee, Edward B.; McMillan, Corey T. (2017-03-16).
826:
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36:
1488:
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859:"Cognitive decline associated with pathological burden in primary age-related tauopathy"
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671:"Comparison of symptomatic and asymptomatic persons with primary age-related tauopathy"
670:
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610:
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527:
494:
470:
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379:
331:
120:
24:
495:"Primary age-related tauopathy (PART): a common pathology associated with human aging"
438:"Primary age-related tauopathy (PART): a common pathology associated with human aging"
405:
1642:
1048:"Current Understanding of Neurodegenerative Diseases Associated With the Protein Tau"
375:
335:
67:
1505:
1132:
275:
growth, retrograde and antegrade transport intracellularly and neuron maintenance.
229:
152:
78:
peptide accumulation in plaques. This ultimately leads to neuronal death and brain
71:
1205:"PART, a distinct tauopathy, different from classical sporadic Alzheimer disease"
1063:
996:
686:
669:
Besser, Lilah M.; Crary, John F.; Mock, Charles; Kukull, Walter A. (2017-10-17).
611:"PART, a distinct tauopathy, different from classical sporadic Alzheimer disease"
320:
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159:
112:
59:
1384:
Proceedings of the
National Academy of Sciences of the United States of America
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131:
Patients with PART can be cognitively normal, mildly cognitively impaired, or
1611:
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1005:
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461:
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Hyper-phosphorylation of tau protein was initially thought to be caused by Aβ
1404:
308:
205:
144:
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1431:
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and cognitively impaired individuals that can occur independently of the
324:
148:
116:
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83:
79:
1333:
863:
Alzheimer's & Dementia: The
Journal of the Alzheimer's Association
799:"The MAPT H1 haplotype is associated with tangle-predominant dementia"
1603:
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261:
63:
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can pass the blood brain barrier and act on HSP90 to inhibit it.
316:
312:
32:
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formation. Also development of specific tau tracers allows for
256:
of brain autopsy of PART cases reveal that NFT's appear in the
323:
and its inhibition resulted in elimination of tau aggregates
411:
linked to
Alzheimer's" Medical news today, November 14, 2014
119:
pathology is sparse or absent in patients with PART. If few
342:. MiRNA-219 binds to tau mRNA and represses tau protein
166:
scans are the only current available diagnostic tools.
980:"Dementia in the oldest old: Beyond Alzheimer disease"
330:
Recent finding's on tau regulation has revealed small
162:
testing cannot be used to identify PART patients and
286:(microtubule polymerization), proline rich domain (
978:Pierce, Aimee L.; Kawas, Claudia H. (2017-03-21).
31:(NFT) that are commonly observed in the brains of
1262:"Alzheimer Mechanisms and Therapeutic Strategies"
278:Tau protein is divided into three segments, i.e.
921:"Tau PET imaging: present and future directions"
183:and consequently its development into NFTs. Aβ
27:designation introduced in 2014 to describe the
319:(HSP90) since HSP90 performs such function in
295:its self and thus ultimately loses function.
8:
1260:Huang, Yadong; Mucke, Lennart (2012-03-16).
1619:
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143:along with tests of processing speed and
151:(cognitive impairment and dementia) and
398:
1581:
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208:and no association has been seen with
1592:The Journal of Clinical Investigation
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910:
338:and silence their expression through
282:(regulated spacing of microtubules),
7:
1530:Acta Neuropathologica Communications
1460:Cellular and Molecular Life Sciences
852:
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431:
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1148:"PART is part of Alzheimer disease"
553:"PART is part of Alzheimer disease"
170:Relationship to Alzheimer's disease
179:presence in AD contributes to tau
45:Columbia University Medical Center
14:
224:has been linked to Parkinson and
1046:Josephs, Keith A. (2017-08-01).
334:bind to recognition motifs on
196:PART has been associated with
1:
340:post-translational regulation
17:Primary age-related tauopathy
1064:10.1016/j.mayocp.2017.04.016
997:10.1371/journal.pmed.1002263
687:10.1212/WNL.0000000000004521
266:positron emission tomography
925:Molecular Neurodegeneration
107:Patients with PART display
1665:
1278:10.1016/j.cell.2012.02.040
875:10.1016/j.jalz.2017.01.028
260:area which is involved in
103:Neuropathological features
1543:10.1186/s40478-016-0406-4
1472:10.1007/s00018-017-2574-1
1221:10.1007/s00401-015-1407-2
1164:10.1007/s00401-015-1390-7
1109:10.1007/s00401-014-1356-1
938:10.1186/s13024-017-0162-3
815:10.1007/s00401-012-1017-1
755:10.1007/s00401-017-1681-2
627:10.1007/s00401-015-1407-2
569:10.1007/s00401-015-1390-7
511:10.1007/s00401-014-1349-0
454:10.1007/s00401-014-1349-0
406:"Researchers identify new
371:Small molecule inhibitors
200:association tau protein (
311:(Thr ), kinases such as
1405:10.1073/pnas.0701055104
1052:Mayo Clinic Proceedings
226:frontotemporal dementia
169:
109:neurofibrillary tangles
47:) and Peter T. Nelson (
29:neurofibrillary tangles
49:University of Kentucky
1209:Acta Neuropathologica
1152:Acta Neuropathologica
1097:Acta Neuropathologica
803:Acta Neuropathologica
743:Acta Neuropathologica
615:Acta Neuropathologica
557:Acta Neuropathologica
499:Acta Neuropathologica
442:Acta Neuropathologica
409:neurological disorder
317:heat shock protein 90
181:hyper phosphorylation
254:Immunohistochemistry
88:cognitive impairment
1396:2007PNAS..104.9511L
1328:(47): 10039–10041.
388:blood brain barrier
41:Alzheimer's disease
250:immunofluorescence
1466:(22): 4159–4169.
1390:(22): 9511–9516.
1334:10.1021/bi1016233
681:(16): 1707–1715.
384:kinase inhibitors
127:Clinical features
92:amnestic dementia
25:neuropathological
1656:
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1604:10.1172/JCI78421
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1272:(6): 1204–1222.
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1058:(8): 1291–1303.
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332:non coding RNAs
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240:Pathophysiology
220:(3R and 4R) on
194:
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141:semantic memory
129:
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37:amyloid plaques
12:
11:
5:
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1598:(2): 681–686.
1575:
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1437:
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1215:(5): 757–762.
1195:
1158:(5): 749–756.
1138:
1103:(6): 767–772.
1087:
1029:
970:
906:
846:
809:(5): 693–704.
786:
749:(5): 705–715.
718:
658:
621:(5): 757–762.
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563:(5): 749–756.
542:
505:(6): 755–766.
485:
448:(6): 755–766.
413:
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380:Methylene blue
372:
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305:Overexpression
299:
292:β-plated sheet
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128:
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121:senile plaques
104:
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66:in the medial
53:Google Scholar
13:
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984:PLOS Medicine
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386:can pass the
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359:HSP90 Targets
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160:serological
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284:C-terminal
280:N-terminal
246:immunoblot
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