Manager, Sydney Brain Bank
+612 9399 1708
Heather has worked for over 20 years in brain banking and neuroscience research and has utilised valuable donor brain tissue to publish a number of neuropathology-focused primary research papers and reviews on a range of neurodegenerative diseases, including Lewy body disease, Alzheimer’s disease, frontotemporal degeneration, multiple system atrophy and myoclonus dystonia. As Manager of the Sydney Brain Bank, her primary roles are overseeing the processing and storage of donated brain and spinal cord tissue with an emphasis on maintaining the highest possible tissue quality and liaising with national and international researchers to provide tissue specimens for merit-based research projects.
Heather has a particular interest in the histopathological analysis of brain and spinal cord tissue, which is essential for the classification of cases and enables careful construction of disease group cohorts.
PROFESSOR GLENDA HALLIDAY SBB Research Neuropathologist
CARLA SCICLUNA Research Assistant
: 9399 1826
To investigate the prevalence of clinically relevant multiple system atrophy (MSA) and Lewy body disease (LBD) pathologies in a large frontotemporal lobar degeneration (FTLD) cohort to determine if concomitant pathologies underlie the heterogeneity of clinical features. Coexisting LBD in FTLD comprises a small proportion of cases but has implications for clinical and neuropathologic diagnoses and the identification of biomarkers.
The location and number of brain stem serotonin-synthesizing neurons were analyzed in 11 patients with Alzheimer's disease (AD) and 5 age-matched controls using immunohistochemical techniques. In addition, the number of neuritic plaques and neurofibrillary tangles in the cortex and brain stem raphe was evaluated, as was the number of Nissl-stained raphe neurons. AD patients could be classified into two groups based on their raphe pathology; patients with such pathology (AD+) and those without (AD-). The number of large raphe neurons correlated significantly with the number of serotonin-synthesizing neurons in control material, indicating that all large neurons were serotonergic. This relationship was not apparent in AD+ patients, in whom the number of serotonin-synthesizing neurons correlated with the number of neurofibrillary tangles in the raphe of these patients. This indicates that in AD+ patients the serotonin-synthesizing neurons were selectively affected. There was no correlation between raphe and cortical pathology or raphe pathology and patient sex, age, mini-mental score or depression score, even when such scores were weighted for the interval between testing and death. There was a trend for the raphe pathology to correlate with the age of onset and duration of dementia and the Blessed dementia score in AD+ patients. Most AD+ patients with severe raphe lesions had clinical dementia only, while AD- patients had additional clinical features. The raphe lesions were more dramatic in AD+ patients with a rapid progression of symptoms.
To investigate the degree of cortical inflammation in dementia with Lewy bodies (DLB) compared with Alzheimer disease (AD) and control brains. Inflammation appears related to the tau neuritic plaques of AD. Despite similar clinical presentations, therapeutic anti-inflammatory strategies are not likely to be effective for pure DLB. Arch Neurol. 2000.