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Intranasal NAP (davunetide) decreases tau hyperphosphorylation and moderately improves behavioral deficits in mice overexpressing α-synuclein.

Pharmacology research & perspectives

Magen I, Ostritsky R, Richter F, Zhu C, Fleming SM, Lemesre V, Stewart AJ, Morimoto BH, Gozes I, Chesselet MF.
PMID: 25505609
Pharmacol Res Perspect. 2014 Oct;2(5):e00065. doi: 10.1002/prp2.65. Epub 2014 Aug 06.

Genome-wide association studies have identified strong associations between the risk of developing Parkinson's disease (PD) and polymorphisms in the genes encoding α-synuclein and the microtubule-associated protein tau. However, the contribution of tau and its phosphorylated form (p-tau) to α-synuclein-induced...

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Magen I, Ostritsky R, Richter F, et al. Intranasal NAP (davunetide) decreases tau hyperphosphorylation and moderately improves behavioral deficits in mice overexpressing α-synuclein. Pharmacol Res Perspect. 2014;2(5):e00065doi: 10.1002/prp2.65.
Magen, I., Ostritsky, R., Richter, F., Zhu, C., Fleming, S. M., Lemesre, V., Stewart, A. J., Morimoto, B. H., Gozes, I., & Chesselet, M. F. (2014). Intranasal NAP (davunetide) decreases tau hyperphosphorylation and moderately improves behavioral deficits in mice overexpressing α-synuclein. Pharmacology research & perspectives, 2(5), e00065. https://doi.org/10.1002/prp2.65
Magen, Iddo, et al. "Intranasal NAP (davunetide) decreases tau hyperphosphorylation and moderately improves behavioral deficits in mice overexpressing α-synuclein." Pharmacology research & perspectives vol. 2,5 (2014): e00065. doi: https://doi.org/10.1002/prp2.65
Magen I, Ostritsky R, Richter F, Zhu C, Fleming SM, Lemesre V, Stewart AJ, Morimoto BH, Gozes I, Chesselet MF. Intranasal NAP (davunetide) decreases tau hyperphosphorylation and moderately improves behavioral deficits in mice overexpressing α-synuclein. Pharmacol Res Perspect. 2014 Oct;2(5):e00065. doi: 10.1002/prp2.65. Epub 2014 Aug 06. PMID: 25505609; PMCID: PMC4186425.
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Impaired baroreflex function in mice overexpressing alpha-synuclein.

Frontiers in neurology

Fleming SM, Jordan MC, Mulligan CK, Masliah E, Holden JG, Millard RW, Chesselet MF, Roos KP.
PMID: 23888153
Front Neurol. 2013 Jul 23;4:103. doi: 10.3389/fneur.2013.00103. eCollection 2013.

Cardiovascular autonomic dysfunction, such as orthostatic hypotension consequent to baroreflex failure and cardiac sympathetic denervation, is frequently observed in the synucleinopathy Parkinson's disease (PD). In the present study, the baroreceptor reflex was assessed in mice overexpressing human wildtype alpha-synuclein...

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Fleming SM, Jordan MC, Mulligan CK, et al. Impaired baroreflex function in mice overexpressing alpha-synuclein. Front Neurol. 2013;4:103doi: 10.3389/fneur.2013.00103.
Fleming, S. M., Jordan, M. C., Mulligan, C. K., Masliah, E., Holden, J. G., Millard, R. W., Chesselet, M. F., & Roos, K. P. (2013). Impaired baroreflex function in mice overexpressing alpha-synuclein. Frontiers in neurology, 4103. https://doi.org/10.3389/fneur.2013.00103
Fleming, Sheila M, et al. "Impaired baroreflex function in mice overexpressing alpha-synuclein." Frontiers in neurology vol. 4 (2013): 103. doi: https://doi.org/10.3389/fneur.2013.00103
Fleming SM, Jordan MC, Mulligan CK, Masliah E, Holden JG, Millard RW, Chesselet MF, Roos KP. Impaired baroreflex function in mice overexpressing alpha-synuclein. Front Neurol. 2013 Jul 23;4:103. doi: 10.3389/fneur.2013.00103. eCollection 2013. PMID: 23888153; PMCID: PMC3719027.
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Alpha-synuclein pathology, microgliosis, and parvalbumin neuron loss in the amygdala associated with enhanced fear in the Thy1-aSyn model of Parkinson's disease.

Neurobiology of disease

Torres ERS, Stanojlovic M, Zelikowsky M, Bonsberger J, Hean S, Mulligan C, Baldauf L, Fleming S, Masliah E, Chesselet MF, Fanselow MS, Richter F.
PMID: 34390837
Neurobiol Dis. 2021 Oct;158:105478. doi: 10.1016/j.nbd.2021.105478. Epub 2021 Aug 11.

In Parkinson's disease (PD), the second most common neurodegenerative disorder, non-motor symptoms often precede the development of debilitating motor symptoms and present a severe impact on the quality of life. Lewy bodies containing misfolded α-synuclein progressively develop in neurons...

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Torres ERS, Stanojlovic M, Zelikowsky M, et al. Alpha-synuclein pathology, microgliosis, and parvalbumin neuron loss in the amygdala associated with enhanced fear in the Thy1-aSyn model of Parkinson's disease. Neurobiol Dis. 2021;158:105478doi: 10.1016/j.nbd.2021.105478.
Torres, E. R. S., Stanojlovic, M., Zelikowsky, M., Bonsberger, J., Hean, S., Mulligan, C., Baldauf, L., Fleming, S., Masliah, E., Chesselet, M. F., Fanselow, M. S., & Richter, F. (2021). Alpha-synuclein pathology, microgliosis, and parvalbumin neuron loss in the amygdala associated with enhanced fear in the Thy1-aSyn model of Parkinson's disease. Neurobiology of disease, 158105478. https://doi.org/10.1016/j.nbd.2021.105478
Torres, Eileen Ruth S, et al. "Alpha-synuclein pathology, microgliosis, and parvalbumin neuron loss in the amygdala associated with enhanced fear in the Thy1-aSyn model of Parkinson's disease." Neurobiology of disease vol. 158 (2021): 105478. doi: https://doi.org/10.1016/j.nbd.2021.105478
Torres ERS, Stanojlovic M, Zelikowsky M, Bonsberger J, Hean S, Mulligan C, Baldauf L, Fleming S, Masliah E, Chesselet MF, Fanselow MS, Richter F. Alpha-synuclein pathology, microgliosis, and parvalbumin neuron loss in the amygdala associated with enhanced fear in the Thy1-aSyn model of Parkinson's disease. Neurobiol Dis. 2021 Oct;158:105478. doi: 10.1016/j.nbd.2021.105478. Epub 2021 Aug 11. PMID: 34390837; PMCID: PMC8447919.
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The etiopathogenesis of Parkinson disease and suggestions for future research. Part I.

Journal of neuropathology and experimental neurology

Litvan I, Halliday G, Hallett M, Goetz CG, Rocca W, Duyckaerts C, Ben-Shlomo Y, Dickson DW, Lang AE, Chesselet MF, Langston WJ, Di Monte DA, Gasser T, Hagg T, Hardy J, Jenner P, Melamed E, Myers RH, Parker D, Price DL.
PMID: 17413315
J Neuropathol Exp Neurol. 2007 Apr;66(4):251-7. doi: 10.1097/nen.0b013e3180415e42.

No abstract available.

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Litvan I, Halliday G, Hallett M, et al. The etiopathogenesis of Parkinson disease and suggestions for future research. Part I. J Neuropathol Exp Neurol. 2007;66(4):251-7doi: 10.1097/nen.0b013e3180415e42.
Litvan, I., Halliday, G., Hallett, M., Goetz, C. G., Rocca, W., Duyckaerts, C., Ben-Shlomo, Y., Dickson, D. W., Lang, A. E., Chesselet, M. F., Langston, W. J., Di Monte, D. A., Gasser, T., Hagg, T., Hardy, J., Jenner, P., Melamed, E., Myers, R. H., Parker, D., & Price, D. L. (2007). The etiopathogenesis of Parkinson disease and suggestions for future research. Part I. Journal of neuropathology and experimental neurology, 66(4), 251-7. https://doi.org/10.1097/nen.0b013e3180415e42
Litvan, Irene, et al. "The etiopathogenesis of Parkinson disease and suggestions for future research. Part I." Journal of neuropathology and experimental neurology vol. 66,4 (2007): 251-7. doi: https://doi.org/10.1097/nen.0b013e3180415e42
Litvan I, Halliday G, Hallett M, Goetz CG, Rocca W, Duyckaerts C, Ben-Shlomo Y, Dickson DW, Lang AE, Chesselet MF, Langston WJ, Di Monte DA, Gasser T, Hagg T, Hardy J, Jenner P, Melamed E, Myers RH, Parker D, Price DL. The etiopathogenesis of Parkinson disease and suggestions for future research. Part I. J Neuropathol Exp Neurol. 2007 Apr;66(4):251-7. doi: 10.1097/nen.0b013e3180415e42. PMID: 17413315.
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Showing 1 to 4 of 4 entries