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Basal activation of astrocytic Nrf2 in neuronal culture media: challenges and implications for neuron-astrocyte modelling (2024)
Preprint / Working Paper
Elsharkasi, M., Villani, B., Wells, G., & Kerr, F. Basal activation of astrocytic Nrf2 in neuronal culture media: challenges and implications for neuron-astrocyte modelling

As a gate-keeper of anti-oxidant, anti-inflammatory and xenobiotic cell protection mechanisms, the transcription factor Nrf2 has been implicated as a promising therapeutic target for several neurodegenerative diseases, leading to the development of N... Read More about Basal activation of astrocytic Nrf2 in neuronal culture media: challenges and implications for neuron-astrocyte modelling.

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., Martinez, P., Callard, R., Snoeren, I., Cochemé, H. M., Adcott, J., Khericha, M., Castillo-Quan, J. I., Wells, G., Noble, W., Thornton, J., & Partridge, L. (2017). Direct Keap1-Nrf2 disruption as a potential therapeutic target for Alzheimer’s disease. PLOS Genetics, 13(3), Article e1006593. 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.

Inhibition of GSK-3 Ameliorates Aβ 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., Allen, M. J., Hardy, J., Lovestone, S., & Partridge, L. (2010). Inhibition of GSK-3 Ameliorates Aβ Pathology in an Adult-Onset Drosophila Model of Alzheimer's Disease. PLOS Genetics, 6(9), Article e1001087. 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 Aβ 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.