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Tasnim attained a Bachelor of Advanced Science at the University of Sydney, with Honours in Physiology (Neuroscience) in 2013. She was awarded a summer scholarship to study cofilin aggregates in the progression of Alzheimer’s disease at the Brain and Mind Research Institute, where she continued as a Research Assistant and published a paper. Tasnim is now pursuing a PhD project looking to establish developmental neurobiological changes in the maternal-immune-activated model of schizophrenia.
Studying the molecular basis of raloxifene (a SERM) modulation of dopamine signalling in schizophrenia, which uses a maternal immune activation rodent model of schizophrenia to better understand how raloxifene brings about its effects.
DEBORA ROTHMOND Senior Research Assistant
: 9399 1846
MIA may alter glutamatergic signaling in cortical and hippocampal regions via alterations in NMDAR indices; however, this was independent of gestational timing. Male MIA offspring have exaggerated changes in NMDAR compared to females in both the cortex and striatum. The MIA-induced increase in NR2A may decrease brain plasticity and contribute to the exacerbated behavioral changes reported in males and indicate that the brains of male offspring are more susceptible to long-lasting changes in glutamate neurotransmission induced by developmental inflammation.
We sought further understanding of the significance of cofilin rods/aggregates to the disease process: Do rods/aggregates correlate with AD progression and the development of hallmark neurofibrillary tangles and neuropil threads? Are cofilin rods/aggregates found in the same neurites as hyperphosphorylated tau? Cofilin rods and aggregates signify events initiated early in the pathological cascade. Further definition of the mechanisms leading to their formation in the human brain will provide insights into the cellular causes of AD.