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All Seminars are held in the Gavin De Beer Lecture Theatre, Anatomy Building, Thursday 1-2pm
Tom Wyatt (Charras lab) "Oriented division in stretched epithelial monolayers"
Ravi Desai (Oates lab) “Micropatterning to interrogate cell biology”
23 Oct: Prof William Wisden, Imperial College
30 Oct: Harold
Burgess , NIH
31 Oct: SPECIAL SEMINAR - Sophie Jarriault (IGBMC) – Title TBC (Host: Dr Richard Poole)
6 Nov: Aude Marzo (Salinas lab)/ Maite Ogueta (Stanewsky lab)
13 Nov: (Paluch lab)/ Robert Bentham (Szabadkai lab)
27 Nov: Irene (Stern lab)/Cristina Benito(Jessen lab)
11 Dec: Marcus Ghosh (Rihel lab)/ (Chubbs lab)
Salinas lab findings on halting Alzheimer's disease in mice published in Journal of Neuroscience
12 March 2012
Professor Patricia Salinas (UCL Department of Cell & Developmental Biology) and her research team have discovered that specific antibodies that block the function of a protein, called Dkk1, are able to completely suppress the toxic effect of Amyloid-ß on synapses. The findings were published last week in the Journal of Neuroscience. Read on for the full story.
Memory loss in Alzheimer's disease could be prevented by targeting a secreted protein that dismantles synapses
Alzheimer’s disease is characterized by abnormal deposits in the brain of the protein Amyloid-ß, which induces the loss of connections between neurons, called synapses. However, the mechanisms that induce synaptic loss are not understood.
Professor Patricia Salinas (UCL Department of Cell & Developmental Biology) and her research team have discovered that specific antibodies that block the function of a protein, called Dkk1, are able to completely suppress the toxic effect of Amyloid-ß on synapses. The findings are published in the Journal of Neuroscience.
Dkk1 is elevated in the brain biopsies of people with Alzheimer’s disease but the significance of these findings was previously unknown. Two members of the Salinas’ group, Drs Silvia Purro and Ellen Dickins, found that Amyloid-ß causes the rapid production of Dkk1, which in turn induces the dismantling of synapses (the connections between neurons) in the hippocampus, an area of the brain implicated in learning and memory. However, specific antibodies against Dkk1 could prevent synaptic loss induced by Amyloid-ß. Neurons that were exposed to the antibody remained healthy, with no synaptic disintegration.
Professor Salinas said: “Despite significant advances in understanding the molecular mechanisms involved in Alzheimer’s disease, no effective treatment is currently available to stop the progression of this devastating disease.” She added: “This research identifies Dkk1 as a potential therapeutic target for the treatment of Alzheimer’s disease.”
The research was funded by Alzheimer’s Research UK, the BBSRC and the Wellcome Trust.
Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said: “We’re delighted to have supported this study”. “Studies like this are an essential part of that process, but more work is needed if we are to take these results from the lab bench to the clinic. Dementia can only be defeated through research, and with the numbers of people affected by the condition soaring, we urgently need to invest in research now.”
Amyloid beta (cyan blue) binds to nerve cells of the hippocampus (red) and attacks synapses resulting in the loss of memories in Alzheimer’s disease. New research has led to important insights into the mechanisms that induce synapse loss. The discovery brings hope for the development of new therapies that protect synapses and therefore prevent memory loss in Alzheimer’s disease.
Credit: Silvia Purro/Patricia Salinas/UCL
Page last modified on 12 mar 12 11:17 by Edward D Whitfield