Quick Project Snapshot

Characterising a mouse model of Acrodermatitis enteropathica

A devastating, lethal genetic disease of zinc metabolism is acrodermatitis enteropathica (AE) which is caused by compromised absorption of dietary zinc. AE symptoms develop after birth in bottle fed infants or after weaning in breast fed infants and patients must be provided lifelong zinc supplementation or they suffer from a myriad of symptoms of severe zinc deficiency which eventually lead to death if not treated with zinc. However, some patients are resistant to zinc supplementation and excess zinc can affect the homeostasis of other essential metals.  Utilising a conditional knockout mouse model of AE we are going to characterise the brain response to zinc deficits, the associated effect on learning and memory and related signalling pathways, and the subsequent benefit that can be achieved through administration of compounds that act to normalise zinc homeostasis.

A/Prof Paul Adlard

Synaptic Neurobiology Laboratory


Our laboratory is interested in understanding the critical role zinc plays at the synapse, as it is critical in learning and memory. This has downstream relevance to a number of different research foci within the lab, including both normal and pathological ageing (e.g. age-related cognitive decline, Alzheimer’s disease and Frontotemporal dementia), as well as to other conditions (such as head trauma) that are characterized by a failure of normal zinc ion homeostasis. Other diseases, such as the zinc-mediated Acrodermatitis enteropathica, are also studied within the lab.

Through close collaboration with Prana Biotechnology, as well as other local and international collaborations, we are exploring how zinc is involved in disease initiation and progression, and how it may itself be a therapeutic target. Thus, we hope to translate our basic science into effective therapeutics for these devastating conditions.

We utilize a number of techniques within the lab, such as in vivo pre-clinical models (animal behaviour, surgery, microdialysis, controlled cortical impact TBI model etc), multielectrode arrays (for high throughput electrophysiology), cell culture (primary cultures, cell lines, microfluidic cultures), synaptic RNA profiling using next generation sequencing and other more standard methodologies such as western blotting and tissue histology, including stereological analysis.

“We invite outstanding PhD candidates to meet and discuss potential projects”.


All Projects by this Lab

Examining local transcriptional profiling of RNA populations in pre- and post-synaptic terminalsUnderstanding the role of metals in normal and pathological ageingCharacterising a mouse model of Acrodermatitis enteropathica


Scientists in the Neurodegeneration division interrogate how neurones live, die and can be rescued to improve brain function in degenerative conditions such as Parkinson’s and Motor Neuron Diseases. There is no effective treatment for Motor Neurone Disease and the incidence of Parkinson’s Disease is rising alarmingly in our aging community. Gene abnormalities, energy deprivation, toxic rubbish accumulation and inflammation all contribute to a toxic environment for brain cells. Our teams study these events in animal models and cultured cells, with a view to translating knowledge into new therapies for human patients.

All Labs that operate in this Division

Atomic Pathology LaboratoryCreutzfeldt Jakob Disease Clinical Research GroupMolecular Gerontology LaboratoryMotor Neurone Disease LaboratoryNational Dementia Diagnostics LaboratoryNeurochemistry of Metal IonsNeurogenesis and Neural Transplantation LaboratoryNeuropathology and Neurodegeneration LaboratoryNeuroproteomics and Metalloproteomics LaboratoryNeurotherapeutics LaboratoryParkinson's Disease LaboratoryPre-clinical Parkinson’s Disease Research LaboratoryPresynaptic Physiology Stem Cells and Neural Development LaboratorySteroid Neurobiology LaboratorySynaptic Neurobiology LaboratoryThe Australian Imaging Biomarker and Lifestyle Study (AIBL)