Senior Principal Research Fellow, NeuRA
Professor of Cognitive Neurology, UNSW
Ex-ARC Federation Fellow
+61 2 9399 1732
John Hodges trained in medicine and psychiatry in London, Southampton and Oxford before gravitating to neurology and becoming enamoured by neuropsychology. In 1990, he was appointed a University Lecturer in Cambridge and in 1997 became MRC Professor of Behaviour Neurology. A sabbatical in Sydney in 2002 with Glenda Halliday rekindled a love of sea, sun and surf which culminated in a move here in 2007 as ARC Federation Fellow and Professor of Cognitive Neurology. He has written 500 papers on aspects of neuropsychology (especially memory and languages) and dementia, plus six books. He co-directs (with Assoc Prof Olivier Piguet) a multidisciplinary research group (Frontier) which focuses on aspects of frontotemporal dementia.
DR CRISTIAN LEYTON Honorary Research Officer
DR EMMA DEVENNEY PhD student
Metabolic changes incorporating fluctuations in weight, insulin resistance, and cholesterol concentrations have been identified in several neurodegenerative disorders. Whether these changes result from the neurodegenerative process affecting brain regions necessary for metabolic regulation or whether they drive the degenerative process is unknown. Emerging evidence from epidemiological, clinical, pathological, and experimental studies emphasises a range of changes in eating behaviours and metabolism in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). In ALS, metabolic changes have been linked to disease progression and prognosis. Furthermore, changes in eating behaviour that affect metabolism have been incorporated into the diagnostic criteria for FTD, which has some clinical and pathological overlap with ALS. Whether the distinct and shared metabolic and eating changes represent a component of the proposed spectrum of the two diseases is an intriguing possibility. Moreover, future research should aim to unravel the complex connections between eating, metabolism, and neurodegeneration in ALS and FTD, and aim to understand the potential for targeting modifiable risk factors in disease development and progression.
To define the severity of abnormal eating behavior and sucrose preference and their neural correlates in patients with behavioral variant FTD (bvFTD) and semantic dementia. Marked hyperphagia is restricted to bvFTD, present in all patients with this diagnosis, and supports its diagnostic value. Differing neural networks control eating behavior in patients with bvFTD and semantic dementia and are likely responsible for the differences seen, with a similar network controlling sucrose preference. These networks share structures that control cognitive-reward, autonomic, neuroendocrine, and visual modulation of eating behavior. Delineating the neural networks involved in mediating these changes in eating behavior may enable treatment of these features in patients with complex medical needs and aid in our understanding of structures that control eating behavior in patients with FTD and healthy individuals.