David Lloyd

RESEARCHER PROFILE

PhD Student

0422 713 515


My academic background is in psychology with a focus on neuroscience and abnormal psychology (e.g. major depression, psychosis). After completing a bachelor’s degree in psychology at Sydney University I completed an honour’s thesis involving the use of a non-invasive brain stimulation tool known as transcranial magnetic stimulation (TMS) aimed at improving the understanding of visual perception in humans.

I am currently completing a PhD thesis at NeuRA, which is focusing on the role of genes, such as Neuregulin 1, and lifestyle factors, such as cannabis use, in relation to their effects on inflammation in the brain that may contribute to schizophrenia.

My investigation into the role of cannabis is performed using mutant mice, which have been genetically altered to mimic genetic changes associated with schizophrenia in humans. These studies have shown that increased activity of the Neuregulin 1 gene can alter the effects of long-term cannabis use in mice, such that cannabis may be able to improve certain aspects of brain function, including association memory, which are originally impaired in the genetically-altered Neuregulin 1 mice, but possibly putting other brain processes at risk. The tests used for mice are minimally stressful and follow strict ethical guidelines.

Projects David Lloyd is currently involved with

CURRENT PROJECTS

The role of genetic factors in the regulation of inflammation in schizophrenia

This research looks at the effects of chronic cannabis on neuroinflammation in the mouse brain, which is part of a larger focus within Cyndi Shannon-Weickert’s lab on neuroinflammatory markers in schizophrenia.

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The role of genetic factors in the regulation of inflammation in schizophrenia

SCIENTISTS CLOSER TO CAUSE OF SCHIZOPHRENIA WITH DRAMATIC GENETIC FINDING

RESEARCH TEAM

PUBLICATIONS

Neuregulin-1 and schizophrenia in the genome-wide association study era.

Mostaid MS, Lloyd D, Liberg B, Sundram S, Pereira A, Pantelis C, Karl T, Weickert CS, Everall IP, Bousman CA

Clinical and pre-clinical evidence has implicated neuregulin 1 (NRG1) as a critical component in the pathophysiology of schizophrenia. However, the arrival of the genome-wide association study (GWAS) era has yielded results that challenge the relevance of NRG1 in schizophrenia due to the absence of a genome-wide significant NRG1 variant associated with schizophrenia. To assess NRG1's relevance to schizophrenia in the GWAS era, we provide a targeted review of recent preclinical evidence on NRG1's role in regulating several aspects of excitatory/inhibitory neurotransmission and in turn schizophrenia risk. We also present a systematic review of the last decade of clinical research examining NRG1 in the context of schizophrenia. We include concise summaries of genotypic variation, gene-expression, protein expression, structural and functional neuroimaging as well as cognitive studies conducted during this time period. We conclude with recommendations for future clinical and preclinical work that we hope will help prioritize a strategy forward to further advance our understanding of the relationship between NRG1 and schizophrenia.

Brain-stimulation induced blindsight: unconscious vision or response bias?

Lloyd DA, Abrahamyan A, Harris JA

A dissociation between visual awareness and visual discrimination is referred to as "blindsight". Blindsight results from loss of function of the primary visual cortex (V1) which can occur due to cerebrovascular accidents (i.e. stroke-related lesions). There are also numerous reports of similar, though reversible, effects on vision induced by transcranial Magnetic Stimulation (TMS) to early visual cortex. These effects point to V1 as the "gate" of visual awareness and have strong implications for understanding the neurological underpinnings of consciousness. It has been argued that evidence for the dissociation between awareness of, and responses to, visual stimuli can be a measurement artifact of the use of a high response criterion under yes-no measures of visual awareness when compared with the criterion free forced-choice responses. This difference between yes-no and forced-choice measures suggests that evidence for a dissociation may actually be normal near-threshold conscious vision. Here we describe three experiments that tested visual performance in normal subjects when their visual awareness was suppressed by applying TMS to the occipital pole. The nature of subjects' performance whilst undergoing occipital TMS was then verified by use of a psychophysical measure (d') that is independent of response criteria. This showed that there was no genuine dissociation in visual sensitivity measured by yes-no and forced-choice responses. These results highlight that evidence for visual sensitivity in the absence of awareness must be analysed using a bias-free psychophysical measure, such as d', In order to confirm whether or not visual performance is truly unconscious.