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Eriksen, Jason L.

https://orcid.org/0000-0003-1549-4165

Mayo Clinic

Jacksonville College

Citations 4

O4–05–01: Methods of cell death and recovery in the rTg4510 and iP301L inducible mouse models of tauopathy
Lewis, Jada , Zehr, Cindy, Andorfer, Cathy, Eriksen, Jason L. , Yue, Mei, Robinson, Todd, Berger, Zdenek , Hanna, Amanda, Janus, Chris, Hutton, Mike, Knight, Joshua A. , Dickson, Dennis W. , McGowan, Eileen

Alzheimer's & Dementia | August 17, 2006 | Volume: 2 | Issue: 3S_Part_3 | Pages: No page available

10.1016/j.jalz.2006.05.327 Get It

P3–293: Tau clearance through protein degradation pathways
Eriksen, Jason L. , Zehr, Cynthia, Berger, Zdenek , Robinson, Todd, Lewis, Jada , Hutton, Michael

Alzheimer's & Dementia | August 17, 2006 | Volume: 2 | Issue: 3S_Part_15 | Pages: No page available

10.1016/j.jalz.2006.05.1562 Get It

S2–02–06: The tauopathies: From genetics to animal models
Hutton, Mike, Melquist, Stacey , Zehr, Cynthia, Eriksen, Jason L. , Stephan, Dietrich A. , Lewis, Jada , Baker, Matthew , McGowan, Eileen , Dickson, Dennis W. , Ashe, Karen H.

Alzheimer's & Dementia | August 17, 2006 | Volume: 2 | Issue: 3S_Part_1 | Pages: No page available

10.1016/j.jalz.2006.05.086 Get It

An inhibitor of tau hyperphosphorylation prevents severe motor impairments in tau transgenic mice
Corre, Sylvie Le, Klafki, Hans‐Wolfgang , Hübinger, Gabriele, Obermeier, Axel, Sahagún, Heidi, Monse, Barbara, Seneci, Pierfausto , Lewis, Jada , Eriksen, Jason L. , Zehr, Cynthia, Yue, Mei, Dickson, Dennis W. , Hutton, Michael , Roder, Hanno M., Plesnila, Nikolaus , McGowan, Eileen , Dickson, Dennis W

Proceedings of the National Academy of Sciences | June 12, 2006 | Volume: 103 | Issue: 25 | Pages: 9673-9678

10.1073/pnas.0602913103 Get It

An orally bioavailable and blood–brain barrier penetrating analog of the kinase inhibitor K252a was able to prevent the typical motor deficits in the tau (P301L) transgenic mouse model (JNPL3) and markedly reduce soluble aggregated hyperphosphorylated tau. However, neurofibrillary tangle counts were not reduced in the successfully treated cohort, suggesting that the main cytotoxic effects of tau are not exerted by neurofibrillary tangles but by lower molecular mass aggregates of tau. Our findings strongly suggest that abnormal tau hyperphosphorylation plays a critical role in the development of tauopathy and suggest a previously undescribed treatment strategy for neurodegenerative diseases involving tau pathology.