Tasmin Rahman

RESEARCHER PROFILE

PhD Student

+61 2 9399 1741


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.

Projects Tasmin Rahman is currently involved with

CURRENT PROJECTS

Neuroinflammation on inhibitory interneurons in frontal cortex of people with schizophrenia

This project focuses on inflammation in the risk of developing schizophrenia phenotypes and worsening neuropathology. The research is investigating whether neuroinflammatory biotypes exacerbate deficits in molecular indices important for inhibitory interneurons in two regions of the frontal cortex in schizophrenia cases

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Neuroinflammation on inhibitory interneurons in frontal cortex of people with schizophrenia

Raloxifene treatment in Maternal Immune Activation 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.

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Raloxifene treatment in Maternal Immune Activation model of Schizophrenia

RESEARCH TEAM

PUBLICATIONS

Effects of Immune Activation during Early or Late Gestation on N-Methyl-d-Aspartate Receptor Measures in Adult Rat Offspring.

Rahman T, Zavitsanou K, Purves-Tyson T, Harms LR, Meehan C, Schall U, Todd J, Hodgson DM, Michie PT, Weickert CS

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.

Cofilin rods and aggregates concur with tau pathology and the development of Alzheimer's disease.

Rahman T, Davies DS, Tannenberg RK, Fok S, Shepherd C, Dodd PR, Cullen KM, Goldsbury C

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.