User profiles for Jennifer M. Pocock

Jennifer Pocock

Institute of Neurology, University College London (UCL)
Verified email at ucl.ac.uk
Cited by 9616

Neurotransmitter receptors on microglia

JM Pocock, H Kettenmann - Trends in neurosciences, 2007 - cell.com
Microglia are the intrinsic immune cells of the brain and express chemokine and cytokine
receptors that interact with the peripheral immune cells. Recent studies have indicated that …

Cannabinoids inhibit neurodegeneration in models of multiple sclerosis

…, DJR Hankey, SJ Jackson, JL Croxford, JM Pocock… - Brain, 2003 - academic.oup.com
Multiple sclerosis is increasingly being recognized as a neurodegenerative disease that is
triggered by inflammatory attack of the CNS. As yet there is no satisfactory treatment. Using …

Stimulation of microglial metabotropic glutamate receptor mGlu2 triggers tumor necrosis factor α-induced neurotoxicity in concert with microglial-derived Fas ligand

…, F Jones, ESFCS Kubota, JM Pocock - Journal of …, 2005 - Soc Neuroscience
Activated microglia may be detrimental to neuronal survival in a number of neurodegenerative
diseases. Thus, strategies that reduce microglial neurotoxicity may have therapeutic …

Microglial genes regulating neuroinflammation in the progression of Alzheimer's disease

…, P Garcia-Reitboeck, J Hardy, JM Pocock - Current opinion in …, 2016 - Elsevier
Neuroinflammation is a pathological hallmark of Alzheimer's disease (AD), and microglia, the
brain's resident phagocyte, are pivotal for the immune response observed in AD. Microglia …

Activation of microglial group III metabotropic glutamate receptors protects neurons against microglial neurotoxicity

DL Taylor, LT Diemel, JM Pocock - Journal of Neuroscience, 2003 - Soc Neuroscience
A reduction in microglial activation and subsequent neurotoxicity may prove critical for
neuroprotection in neurodegenerative diseases. We examined the expression and functionality of …

Microglia release activators of neuronal proliferation mediated by activation of mitogen‐activated protein kinase, phosphatidylinositol‐3‐kinase/Akt and delta–Notch …

SC Morgan, DL Taylor, JM Pocock - Journal of neurochemistry, 2004 - Wiley Online Library
Microglia, the resident macrophage of the brain, can release substances that aid neuronal
development, differentiation and survival. We have investigated the effects of non‐activated …

[HTML][HTML] Insights into TREM2 biology by network analysis of human brain gene expression data

…, JM Pocock, R Guerreiro, ME Weale, M Ryten - Neurobiology of …, 2013 - Elsevier
Rare variants in TREM2 cause susceptibility to late-onset Alzheimer's disease. Here we use
microarray-based expression data generated from 101 neuropathologically normal …

A genetic link between risk for Alzheimer's disease and severe COVID-19 outcomes via the OAS1 gene

…, C Sala Frigerio, V Escott-Price, K Morgan, JM Pocock… - Brain, 2021 - academic.oup.com
Recently, we reported oligoadenylate synthetase 1 (OAS1) contributed to the risk of Alzheimer’s
disease, by its enrichment in transcriptional networks expressed by microglia. However, …

[PDF][PDF] Human induced pluripotent stem cell-derived microglia-like cells harboring TREM2 missense mutations show specific deficits in phagocytosis

…, S Neame, H Houlden, J Hardy, JM Pocock - Cell Reports, 2018 - cell.com
Dysfunction of microglia, the brain's immune cells, is linked to neurodegeneration.
Homozygous missense mutations in TREM2 cause Nasu-Hakola disease (NHD), an early-onset …

[HTML][HTML] The Trem2 R47H Alzheimer's risk variant impairs splicing and reduces Trem2 mRNA and protein in mice but not in humans

…, M Colonna, J Herms, W Wurst, JM Pocock… - Molecular …, 2018 - Springer
Background The R47H variant of the Triggering Receptor Expressed on Myeloid cells 2 (TREM2)
significantly increases the risk for late onset Alzheimer’s disease. Mouse models …