Direct Keap1-Nrf2 disruption as a potential therapeutic target for Alzheimer’s disease (2017)
Journal Article
Kerr, F., Sofola-Adesakin, O., Ivanov, D. K., Gatliff, J., Gomez Perez-Nievas, B., Bertrand, H. C., …Partridge, L. (2017). Direct Keap1-Nrf2 disruption as a potential therapeutic target for Alzheimer’s disease. PLoS Genetics, 13(3), https://doi.org/10.1371/journal.pgen.1006593

Nrf2, a transcriptional activator of cell protection genes, is an attractive therapeutic target for the prevention of neurodegenerative diseases, including Alzheimer’s disease (AD). Current Nrf2 activators, however, may exert toxicity and pathway ove... Read More about Direct Keap1-Nrf2 disruption as a potential therapeutic target for Alzheimer’s disease.

Deletion of endogenous Tau proteins is not detrimental in Drosophila (2016)
Journal Article
Burnouf, S., Grönke, S., Augustin, H., Dols, J., Gorsky, M. K., Werner, J., …Partridge, L. (2016). Deletion of endogenous Tau proteins is not detrimental in Drosophila. Scientific Reports, 6, https://doi.org/10.1038/srep23102

Human Tau (hTau) is a highly soluble and natively unfolded protein that binds to microtubules within neurons. Its dysfunction and aggregation into insoluble paired helical filaments is involved in the pathogenesis of Alzheimer’s disease (AD), constit... Read More about Deletion of endogenous Tau proteins is not detrimental in Drosophila.

Inhibition of GSK-3 Ameliorates A? Pathology in an Adult-Onset Drosophila Model of Alzheimer's Disease (2010)
Journal Article
Sofola, O., Kerr, F., Rogers, I., Killick, R., Augustin, H., Gandy, C., …Partridge, L. (2010). Inhibition of GSK-3 Ameliorates Aβ Pathology in an Adult-Onset Drosophila Model of Alzheimer's Disease. PLoS Genetics, 6(9), https://doi.org/10.1371/journal.pgen.1001087

Aβ peptide accumulation is thought to be the primary event in the pathogenesis of Alzheimer's disease (AD), with downstream neurotoxic effects including the hyperphosphorylation of tau protein. Glycogen synthase kinase-3 (GSK-3) is increasingly impli... Read More about Inhibition of GSK-3 Ameliorates A? Pathology in an Adult-Onset Drosophila Model of Alzheimer's Disease.

Dietary restriction delays aging, but not neuronal dysfunction, in Drosophila models of Alzheimer's disease (2009)
Journal Article
Kerr, F., Augustin, H., Piper, M. D. W., Gandy, C., Allen, M. J., Lovestone, S., & Partridge, L. (2011). Dietary restriction delays aging, but not neuronal dysfunction, in Drosophila models of Alzheimer's disease. Neurobiology of Aging, 32(11), 1977-1989. https://doi.org/10.1016/j.neurobiolaging.2009.10.015

Dietary restriction (DR) extends lifespan in diverse organisms and, in animal and cellular models, can delay a range of aging-related diseases including Alzheimer's disease (AD). A better understanding of the mechanisms mediating these interactions,... Read More about Dietary restriction delays aging, but not neuronal dysfunction, in Drosophila models of Alzheimer's disease.

PTEN, a negative regulator of PI3 kinase signalling, alters tau phosphorylation in cells by mechanisms independent of GSK-3 (2006)
Journal Article
Kerr, F., Rickle, A., Nayeem, N., Brandner, S., Cowburn, R. F., & Lovestone, S. (2006). PTEN, a negative regulator of PI3 kinase signalling, alters tau phosphorylation in cells by mechanisms independent of GSK-3. FEBS Letters, 580(13), 3121-3128. https://doi.org/10.1016/j.febslet.2006.04.064

Deregulation of PTEN/Akt signalling has been recently implicated in the pathogenesis of Alzheimer's disease (AD), but the effects on the molecular processes underlying AD pathology have not yet been fully described. Here we report that overexpression... Read More about PTEN, a negative regulator of PI3 kinase signalling, alters tau phosphorylation in cells by mechanisms independent of GSK-3.

Glycogen synthase kinase-3 is increased in white cells early in Alzheimer's disease (2004)
Journal Article
Hye, A., Kerr, F., Archer, N., Foy, C., Poppe, M., Brown, R., …Lovestone, S. (2004). Glycogen synthase kinase-3 is increased in white cells early in Alzheimer's disease. Neuroscience Letters, 373(1), 1-4. https://doi.org/10.1016/j.neulet.2004.10.031

Alzheimer's disease (AD) is a disorder without a molecular marker in peripheral tissues or a disease modifying treatment. As increasing evidence has suggested a role for glycogen synthase kinase-3 (GSK-3) in the pathogenesis of the condition we measu... Read More about Glycogen synthase kinase-3 is increased in white cells early in Alzheimer's disease.