scholarly journals Employing an in vitro biosensor assay to investigate tau seeding kinetics within cases of sporadic Alzheimer disease and in a model of tauopathy

2020 ◽  
Vol 16 (S3) ◽  
Author(s):  
Tarun V Kamath ◽  
Caitlin Commins ◽  
Naomi Klickstein ◽  
Derek Oakley ◽  
Bradley T Hyman ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Sporadic Alzheimer Disease

Possible association of mitochondrial transcription factor A (TFAM) genotype with sporadic Alzheimer disease

2004 ◽  
Vol 369 (3) ◽  
pp. 219-223 ◽  
Author(s):  
Claudia Günther ◽  
Kirsten von Hadeln ◽  
Tomas Müller-Thomsen ◽  
Antonella Alberici ◽  
Giuliano Binetti ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Alzheimer Disease ◽  
Mitochondrial Transcription ◽  
Mitochondrial Transcription Factor ◽  
Mitochondrial Transcription Factor A ◽  
Sporadic Alzheimer Disease

Biologic distinction between sporadic and familial Alzheimer disease by an in vitro cell fusion test

Neurology ◽  
1981 ◽  
Vol 31 (3) ◽  
pp. 323-323 ◽  
Author(s):  
M.-C. Moreau-Dubois ◽  
P. Brown ◽  
J. Goudsmit ◽  
F. Cathala ◽  
D. C. Gajdusek
Keyword(s):  
Alzheimer Disease ◽  
Cell Fusion ◽  
Familial Alzheimer Disease

S182 and STM2 gene missense mutations in sporadic Alzheimer disease

1996 ◽  
Vol 67 (4) ◽  
pp. 429-429 ◽  
Author(s):  
Susumu Higuchi ◽  
Sachio Matsushita ◽  
Yoshio Hasegawa ◽  
Taro Muramatsu ◽  
Shigeru Itabashi ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Missense Mutations ◽  
Sporadic Alzheimer Disease

scholarly journals In-vitro evaluation of selected Egyptian traditional herbal medicines for treatment of alzheimer disease

2013 ◽  
Vol 13 (1) ◽  
Author(s):  
Shereen K Ali ◽  
Ahmed R Hamed ◽  
Maha M Soltan ◽  
Usama M Hegazy ◽  
Esameldin E Elgorashi ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Herbal Medicines ◽  
In Vitro Evaluation

scholarly journals PART, a distinct tauopathy, different from classical sporadic Alzheimer disease

2015 ◽  
Vol 129 (5) ◽  
pp. 757-762 ◽  
Author(s):  
Kurt A. Jellinger ◽  
Irina Alafuzoff ◽  
Johannes Attems ◽  
Thomas G. Beach ◽  
Nigel J. Cairns ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Sporadic Alzheimer Disease

NPY modulates miR-30a-5p and BDNF in opposite direction in an in vitro model of Alzheimer disease: a possible role in neuroprotection?

2013 ◽  
Vol 376 (1-2) ◽  
pp. 189-195 ◽  
Author(s):  
Nicoletta Croce ◽  
Francesca Gelfo ◽  
Maria Teresa Ciotti ◽  
Giorgio Federici ◽  
Carlo Caltagirone ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Opposite Direction ◽  
In Vitro Model ◽  
Vitro Model

Scattering differentiates Alzheimer disease in vitro

2008 ◽  
Vol 33 (6) ◽  
pp. 624 ◽  
Author(s):  
Eugene B. Hanlon ◽  
Lev T. Perelman ◽  
Eduard I. Vitkin ◽  
Frank A. Greco ◽  
Ann C. McKee ◽  
...  
Keyword(s):  
Alzheimer Disease

scholarly journals Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease

2011 ◽  
Vol 16 (3) ◽  
Author(s):  
Vladan Bajić ◽  
Bo Su ◽  
Hyoung-Gon Lee ◽  
Wataru Kudo ◽  
Sandra Siedlak ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Alzheimer Disease ◽  
Expression Patterns ◽  
Vital Role ◽  
Dependent Manner ◽  
Entry Site ◽  
Internal Ribosome Entry ◽  
Cellular Processes ◽  
M Phase

AbstractPost-mitotic neurons are typically terminally differentiated and in a quiescent status. However, in Alzheimer disease (AD), many neurons display ectopic re-expression of cell cycle-related proteins. Cyclin-dependent kinase 11 (CDK11) mRNA produces a 110-kDa protein (CDK11p110) throughout the cell cycle, a 58-kDa protein (CDK11p58) that is specifically translated from an internal ribosome entry site and expressed only in the G2/M phase of the cell cycle, and a 46-kDa protein (CDK11p46) that is considered to be apoptosis specific. CDK11 is required for sister chromatid cohesion and the completion of mitosis. In this study, we found that the expression patterns of CDK11 vary such that cytoplasmic CDK11 is increased in AD cellular processes, compared to a pronounced nuclear expression pattern in most controls. We also investigated the effect of amyloid precursor protein (APP) on CDK11 expression in vitro by using M17 cells overexpressing wild-type APP and APP Swedish mutant phenotype and found increased CDK11 expression compared to empty vector. In addition, amyloid-β25–35 resulted in increased CDK11 in M17 cells. These data suggest that CDK11 may play a vital role in cell cycle re-entry in AD neurons in an APP-dependent manner, thus presenting an intriguing novel function of the APP signaling pathway in AD.

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