TCN Lab graduate student, Ben Phillips, has been awarded an Oon Khye Beng Ch’Hia Tsio Studentship by Downing College.
Oon Khye Beng Ch'hia Tsio Studentships are awarded to students who are pursuing biomedical research. The Studentships support them in their research by, for example, enabling them to participate in conferences, or take up internships with overseas health agencies.
Congratulations to Dr Lisa Saksida, whose academic promotion was recently announced in the Cambridge University Reporter (No 6390, Wednesday 10 June 2015). Lisa, who is currently Reader in Cognitive Neuroscience, is to be promoted to Professor with effect from 1 October 2015.
Lisa is one of the two Principal Investigators in the TCN Lab. She researches the fundamental psychological processes involved in memory and perception. Lisa's research encompasses a variety of experimental methods, includes several species, and uses healthy and brain-damaged subjects.
This Sunday, 8th March, Professor Tim Bussey will host a session that celebrates women scientists and the difference their scientific contributions have made to the world.
Tim's session, Wonderwomen: Discoverers and Pioneers, will run from 13:30 to 14:30 at the Junction, and is part of this year's Women of the World (WOW) Festival in Cambridge. Tim will be joined by Professor Monica Grady, Deborah Jaffé, Aurelia Hibbert, and Dr Jenny Tillotson.
Dr Lisa Saksida, was a guest on Chris Berrow's show on BBC Radio Cambridgeshire yesterday afternoon (Wednesday 4 March). The main topic under discussion was dementia. Lisa, whose research interests include the psychological processes underlying memory, explains how different types of memory are affected differentially in dementia. She emphasises the importance of detecting dementia early, and describes how researchers are focussing on developing cognitive tests to allow earlier detection. Lisa also talks about her life as a scientist, and her love of Ashtanga yoga.
The show is available on BBC iPlayer Radio; listen from 2.10 to 2.45 to hear Lisa, and her fellow guest, the author and Alzheimer’s Research UK blogger, Chris Carling, in conversation with Chris Berrow.
Questions posed included 'What one thing don't your students or colleagues know about you?' The fact that Tim is a musician, and lead singer of a pop group, is something most of his students and colleagues have only recently discovered...
From the Nature Protocols Website: The touchscreen operant platform enables assessment of cognitive function in rodents such as mice and rats. It enables tests to be run similarly to touchscreen methods used to test human subjects. These three protocols describe how to use this platform to test learning and memory, executive function, working memory and pattern separation.
Horner, A.E., Heath, C.J., Hvoslef-Eide, M., Kent, B.A., Kim, C.H., Nilsson, S., Alsiö, J., Oomen, C.A., Holmes, A., Saksida, L.M., & Bussey, T.J. (2013) The touchscreen operant platform for testing learning and memory in rats and mice. Nature Protocols, 8(10):1961-84. details pdf
Mar, A.C., Horner, A.E., Nilsson, S., Alsiö, J., Kent, B.A., Kim, C.H., Holmes, A., Saksida, L.M., & Bussey, T.J. (2013) The touchscreen operant platform for assessing executive function in rats and mice. Nature Protocols, 8(10):1985-2005. details pdf
Oomen, C.A., Hvoslef-Eide, M., Heath, C.J., Mar, A.C., Horner, A.E., Bussey, T.J., & Saksida, L.M. (2013) The touchscreen operant platform for testing working memory and pattern separation in rats and mice. Nature Protocols, 8(10):2006-21. details pdf
Also see Michael Ryan Hunsaker's blog for some discussion of these protocols.
The same genes that gave rise to higher mental function are also responsible for a number of brain disorders, the results reveal, suggesting that the evolution of intelligence came at the cost of mental illness.
The discovery pinpoints when in history the genes that enable us to think and reason evolved, giving us the ability to learn complex skills, analyse situations and have flexibility in how we think.
A team led by researchers at the University of Edinburgh used a combination of human and mouse behavioural studies and analysed the underlying genetics to work out how and when certain behaviours evolved.
Their findings trace back the evolution of higher cognitive functions to an increase in the number of copies of specific genes that are involved in signalling processes in the brain. The evidence suggests that the increase occurred as the result of two genetic duplication events in one of our evolutionary ancestors some 500 million years ago. Having the extra copies led descendants of this primitive animal to become more behaviourally sophisticated.
Both humans and mice were used in the study and were given comparative tasks to perform, involving identifying images on computer touchscreen tablets. The research reveals that higher mental functions are controlled by the same genes in both humans and mice, showing that the roles of these genes in cognition were already in place 100 million years ago when the two species last shared a common ancestor.
The study also found that when these genes were mutated or damaged, they interfered with higher mental functions. Professor Seth Grant of the University of Edinburgh, who led the research, explained: "Our work shows that the price of higher intelligence and more complex behaviours is more mental illness."
The researchers had previously shown that more than 100 childhood and adult brain diseases are caused by gene mutations.
"We can now apply genetics and behavioural testing to help patients with these diseases," said Dr Tim Bussey from the University of Cambridge, who was also involved in the study.
"Using the latest molecular and behavioural techniques, this research makes a significant step forward in our understanding of how sophisticated behaviours emerged in humans and other animals," said John Williams, Head of Neuroscience and Mental Health at the Wellcome Trust. "This ground-breaking work has implications for how we understand the emergence of psychiatric disorders and will offer new avenues for the development of new treatments."
The study was funded by the European Union, the Medical Research Council and the Wellcome Trust.
Image: A human brain. Credit: Heidi Cartwright/Wellcome Images
Nithianantharajah J et al. Synaptic scaffold evolution generated components of vertebrate cognitive complexity. Nat Neurosci 2012 [epub].
Ryan TJ et al. Genetic exchange of evolutionarily derived GluN2A and GluN2B cytoplasmic domains identifies shared and unique contributions to vertebrate behavior and synaptic plasticity. Nat Neurosci 2012 [epub].
New TCNLab papers in Journal of Neuroscience, Neurobiology of Aging and Neuroscience and Biobehavioral Reviews.
Cowell, R.A., Bussey, T.J. & Saksida, L.M. (2012). Empiricists are from Venus, Modelers are from Mars: Reconciling Experimental and Computational Approaches in Cognitive Neuroscience. Neuroscience and Biobehavioral Reviews, in press. details
Coba, M.P., Komiyama, N.H., Nithianantharajah, J., Kopanitsa, M.V., Indersmitten, T., Skene, N.G., Tuck, E.J., Fricker, D.G., Elsegood, K.A., Stanford, L.E., Afinowi, N., Saksida, L.M., Bussey, T.J., O’Dell, T.J. & Grant, S.G.N. (2012) TNIK is required for postsynaptic and nuclear signalling pathways and cognitive function. Journal of Neuroscience, i32(40):13987-13999. details
Romberg, C., Horner, A.E., Bussey, T.J. & Saksida, L.M. (2012) A touchscreen-automated cognitive test battery reveals impaired attention, memory abnormalities and increased response inhibition in the TgCRND8 mouse model of Alzheimer's disease. Neurobiology of Aging, in press. details
Barense, M.D., Groen, I.I.A., Lee, A.C.H., Yeung, L-K, Brady, S.M., Gregori, M., Kapur, N., Bussey, T.J., Saksida, L.M.* & Henson, R.N.A.* (2012). Intact memory for irrelevant information impairs perception in amnesia. Neuron, 75(1):157-167.
Memory and perception have long been considered separate cognitive processes, and amnesia resulting from medial temporal lobe (MTL) damage is thought to reflect damage to a dedicated memory system. Recent work has questioned these views, suggesting that amnesia can result from impoverished perceptual representations in the MTL, causing an increased susceptibility to interference. Using a perceptual matching task for which fMRI implicated a specific MTL structure, the perirhinal cortex, we show that amnesics with MTL damage including the perirhinal cortex, but not those with damage limited to the hippocampus, were vulnerable to object-based perceptual interference. Importantly, when we controlled such interference, their performance recovered to normal levels. These findings challenge prevailing conceptions of amnesia, suggesting that effects of damage to specific MTL regions are better understood not in terms of damage to a dedicated declarative memory system, but in terms of impoverished representations of the stimuli those regions maintain. details
who successfully defended her PhD thesis yesterday afternoon. Well done, Dr McAllister!
New TCNLab paper in Journal of Cognitive Neuroscience. Multiple Cognitive Abilities from a Single Cortical Algorithm.
Forwood SE, Cowell R, Bussey T.J., Saksida L.M. Multiple Cognitive Abilities from a Single Cortical Algorithm. J Cogn Neurosci. 2012 May 25.
One strong claim made by the representational-hierarchical account of cortical function in the ventral visual stream (VVS) is that the VVS is a functional continuum: The basic computations carried out in service of a given cognitive function, such as recognition memory or visual discrimination, might be the same at all points along the VVS. Here, we use a single-layer computational model with a fixed learning mechanism and set of parameters to simulate a variety of cognitive phenomena from different parts of the functional continuum of the VVS: recognition memory, categorization of perceptually related stimuli, perceptual learning of highly similar stimuli, and development of retinotopy and orientation selectivity. The simulation results indicate-consistent with the representational-hierarchical view-that the simple existence of different levels of representational complexity in different parts of the VVS is sufficient to drive the emergence of distinct regions that appear to be specialized for solving a particular task, when a common neurocomputational learning algorithm is assumed across all regions. Thus, our data suggest that it is not necessary to invoke computational differences to understand how different cortical regions can appear to be specialized for what are considered to be very different psychological functions.
New TCNLab paper in Brain. False recognition in a mouse model of Alzheimer’s disease: rescue with sensory restriction and memantine.
Romberg, C., McTighe, S.M., Heath, C.J., Whitcomb, D., Cho, K., Bussey, T.J. & Saksida, L.M. (2012) False recognition in a mouse model of Alzheimer’s disease: rescue with sensory restriction and memantine. Brain, in press.
Alzheimer’s disease is commonly regarded as a loss of memory for past events. However, patients with Alzheimer’s disease seem not only to forget events but also to express false confidence in remembering events that have never happened. How and why false recognition occurs in such patients is currently unknown, and treatments targeting this specific mnemonic abnormality have not been attempted. Here, we used a modified object recognition paradigm to show that the tgCRND8 mouse—which overexpresses amyloid b and develops amyloid plaques similar to those in the brains of patients with Alzheimer’s disease— exhibits false recognition. Furthermore, we found that false recognition did not occur when tgCRND8 mice were kept in a dark, quiet chamber during the delay, paralleling previous findings in patients with mild cognitive impairment, which is often con- sidered to be prodromal Alzheimer’s disease. Additionally, false recognition did not occur when mice were treated with the partial N-methyl-D-aspartic acid receptor antagonist memantine. In a subsequent experiment, we found abnormally enhanced N-methyl-D-aspartic acid receptor-dependent long-term depression in these mice, which could be normalized by treatment with memantine. We suggest that Alzheimer’s disease typical amyloid b pathology leads to aberrant synaptic plasticity, thereby making memory representations more susceptible to interfering sensory input, thus increasing the likelihood of false recogni- tion. Parallels between these findings and those from the literature on Alzheimer’s disease and mild cognitive impairment suggest a mechanism underlying false recognition in these patients. The false recognition phenomenon may provide a novel paradigm for the discovery of potential therapies to treat the mnemonic dysfunction characteristic of this disease.
Welcome to our new website! It is currently under construction but should be complete in the next week or so, so please come back soon.
Welcome to the two newest additions to the TCNLab! Chi Hun Kim is here from Seoul, and will be working on a PhD in the area of models of Alzheimer's Disease for the next 3 years. Jytte van Huijstee joins us from Amsterdam; she will be here for several months on a research project as part of her undergraduate degree.