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All Outputs (19)

Creating connections: developing an online space for cross-regional mentorship and network building in the dementia research field [Version 2] (2022)
Journal Article
Fullerton, J., Bettencourt, C., Daniels, M., Mclean, F., Simpson, S., Smith, A., …Kerr, F. (2022). Creating connections: developing an online space for cross-regional mentorship and network building in the dementia research field [Version 2]. AMRC Open Research, 4, Article 22. https://doi.org/10.12688/amrcopenres.13091.2

Background Effective development and retention of talented early-career researchers (ECRs) is essential to the continued success of biomedical science research fields. To this end, formal mentorship programmes (where researchers are paired with one... Read More about Creating connections: developing an online space for cross-regional mentorship and network building in the dementia research field [Version 2].

Building a Systematic Online Living Evidence Summary of COVID-19 Research (2021)
Journal Article
Hair, K., Sena, E. S., Wilson, E., Currie, G., Macleod, M., Bahor, Z., …Drury, B. (2021). Building a Systematic Online Living Evidence Summary of COVID-19 Research. Journal of the European Association for Health Information and Libraries, 17(2), 21-26. https://doi.org/10.32384/jeahil17465

Throughout the global coronavirus pandemic, we have seen an unprecedented volume of COVID-19 researchpublications. This vast body of evidence continues to grow, making it difficult for research users to keep up with the pace of evolving research find... Read More about Building a Systematic Online Living Evidence Summary of COVID-19 Research.

Activating transcription factor 4-dependent lactate dehydrogenase activation as a protective response to amyloid beta toxicity (2021)
Journal Article
Niccoli, T., Kerr, F., Snoeren, I., Fabian, D., Aleyakpo, B., Ivanov, D., …Partridge, L. (2021). Activating transcription factor 4-dependent lactate dehydrogenase activation as a protective response to amyloid beta toxicity. Brain Communications, 3(2), Article fcab053. https://doi.org/10.1093/braincomms/fcab053

Accumulation of amyloid beta peptides is thought to initiate the pathogenesis of Alzheimer’s disease. However, the precise mechanisms mediating their neurotoxicity are unclear. Our microarray analyses show that, in Drosophila models of amyloid beta 4... Read More about Activating transcription factor 4-dependent lactate dehydrogenase activation as a protective response to amyloid beta toxicity.

Dynamic changes in the brain protein interaction network correlates with progression of Aβ42 pathology in Drosophila (2020)
Journal Article
Scholes, H. M., Cryar, A., Kerr, F., Sutherland, D., Gethings, L. A., Vissers, J. P. C., …Thalassinos, K. (2020). Dynamic changes in the brain protein interaction network correlates with progression of Aβ42 pathology in Drosophila. Scientific Reports, 10(1), Article 18517 (2020). https://doi.org/10.1038/s41598-020-74748-9

Alzheimer’s disease (AD), the most prevalent form of dementia, is a progressive and devastating neurodegenerative condition for which there are no effective treatments. Understanding the molecular pathology of AD during disease progression may identi... Read More about Dynamic changes in the brain protein interaction network correlates with progression of Aβ42 pathology in Drosophila.

Molecular Mechanisms of Lithium Action: Switching the Light on Multiple Targets for Dementia Using Animal Models (2018)
Journal Article
Kerr, F., Bjedov, I., & Sofola-Adesakin, O. (2018). Molecular Mechanisms of Lithium Action: Switching the Light on Multiple Targets for Dementia Using Animal Models. Frontiers in Molecular Neuroscience, 11, Article 297. https://doi.org/10.3389/fnmol.2018.00297

Lithium has long been used for the treatment of psychiatric disorders, due to its robust beneficial effect as a mood stabilizing drug. Lithium’s effectiveness for improving neurological function is therefore well-described, stimulating the investigat... Read More about Molecular Mechanisms of Lithium Action: Switching the Light on Multiple Targets for Dementia Using Animal Models.

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), 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.

Increased Glucose Transport into Neurons Rescues Aβ Toxicity in Drosophila (2016)
Journal Article
Niccoli, T., Cabecinha, M., Tillmann, A., Kerr, F., Wong, C., Cardenes, D., …Partridge, L. (2016). Increased Glucose Transport into Neurons Rescues Aβ Toxicity in Drosophila. Current Biology, 26(17), 2291-2300. https://doi.org/10.1016/j.cub.2016.07.017

Glucose hypometabolism is a prominent feature of the brains of patients with Alzheimer's disease (AD). Disease progression is associated with a reduction in glucose transporters in both neurons and endothelial cells of the blood-brain barrier. Howeve... Read More about Increased Glucose Transport into Neurons Rescues Aβ Toxicity in Drosophila.

Lithium Promotes Longevity through GSK3/NRF2-Dependent Hormesis (2016)
Journal Article
Castillo-Quan, J., Li, L., Kinghorn, K., Ivanov, D., Tain, L., Slack, C., …Partridge, L. (2016). Lithium Promotes Longevity through GSK3/NRF2-Dependent Hormesis. Cell Reports, 15(3), 638-650. https://doi.org/10.1016/j.celrep.2016.03.041

The quest to extend healthspan via pharmacological means is becoming increasingly urgent, both from a health and economic perspective. Here we show that lithium, a drug approved for human use, promotes longevity and healthspan. We demonstrate that li... Read More about Lithium Promotes Longevity through GSK3/NRF2-Dependent Hormesis.

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, Article 23102. 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.

A holidic medium for Drosophila melanogaster (2013)
Journal Article
Piper, M. D. W., Blanc, E., Leitão-Gonçalves, R., Yang, M., He, X., Linford, N. J., …Partridge, L. (2014). A holidic medium for Drosophila melanogaster. Nature methods, 11(1), 100-105. https://doi.org/10.1038/nmeth.2731

A critical requirement for research using model organisms is a well-defined and consistent diet. There is currently no complete chemically defined (holidic) diet available for Drosophila melanogaster. We describe a holidic medium that is equal in per... Read More about A holidic medium for Drosophila melanogaster.

Ageing Increases Vulnerability to Aβ42 Toxicity in Drosophila (2012)
Journal Article
Rogers, I., Kerr, F., Martinez, P., Hardy, J., Lovestone, S., & Partridge, L. (2012). Ageing Increases Vulnerability to Aβ42 Toxicity in Drosophila. PLOS ONE, 7(7), Article e40569. https://doi.org/10.1371/journal.pone.0040569

Age is the major risk factor for many neurodegenerative diseases, including Alzheimer's Disease (AD), for reasons that are not clear. The association could indicate that the duration or degree of exposure to toxic proteins is important for pathology,... Read More about Ageing Increases Vulnerability to Aβ42 Toxicity in Drosophila.

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., …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.

Mechanisms of Life Span Extension by Rapamycin in the Fruit Fly Drosophila melanogaster (2010)
Journal Article
Bjedov, I., Toivonen, J. M., Kerr, F., Slack, C., Jacobson, J., Foley, A., & Partridge, L. (2010). Mechanisms of Life Span Extension by Rapamycin in the Fruit Fly Drosophila melanogaster. Cell Metabolism, 11(1), 35-46. https://doi.org/10.1016/j.cmet.2009.11.010

The target of rapamycin (TOR) pathway is a major nutrient-sensing pathway that, when genetically downregulated, increases life span in evolutionarily diverse organisms including mammals. The central component of this pathway, TOR kinase, is the targe... Read More about Mechanisms of Life Span Extension by Rapamycin in the Fruit Fly Drosophila melanogaster.

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.

Deletion of Irs2 reduces amyloid deposition and rescues behavioural deficits in APP transgenic mice (2009)
Journal Article
Killick, R., Scales, G., Leroy, K., Causevic, M., Hooper, C., Irvine, E. E., …Lovestone, S. (2009). Deletion of Irs2 reduces amyloid deposition and rescues behavioural deficits in APP transgenic mice. Biochemical and Biophysical Research Communications, 386(1), 257-262. https://doi.org/10.1016/j.bbrc.2009.06.032

As impaired insulin signalling (IIS) is a risk factor for Alzheimer's disease we crossed mice (Tg2576) over-expressing human amyloid precursor protein (APP), with insulin receptor substrate 2 null (Irs2(-/-)) mice which develop insulin resistance. Th... Read More about Deletion of Irs2 reduces amyloid deposition and rescues behavioural deficits in APP transgenic mice.

Hyperphosphorylation of tau and neurofilaments and activation of CDK5 and ERK1/2 in PTEN-deficient cerebella (2007)
Journal Article
Nayeem, N., Kerr, F., Naumann, H., Linehan, J., Lovestone, S., & Brandner, S. (2007). Hyperphosphorylation of tau and neurofilaments and activation of CDK5 and ERK1/2 in PTEN-deficient cerebella. Molecular and Cellular Neuroscience, 34(3), 400-408. https://doi.org/10.1016/j.mcn.2006.11.014

Inherited mutations to the tumor suppressor PTEN sporadically lead to cerebellar gangliocytoma characterized by migration defects. This has been modeled by CNS-specific PTEN ablation in mice, but the underlying mechanism cannot be explained by the kn... Read More about Hyperphosphorylation of tau and neurofilaments and activation of CDK5 and ERK1/2 in PTEN-deficient cerebella.

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.