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

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

CAITLIN MURPHY PhD student

Duncan Sinclair

DR DUNCAN SINCLAIR Postdoctoral Fellow

Debora Rothmond

DEBORA ROTHMOND Senior Research Assistant

Shan Tsai

SHAN-YUAN TSAI-CHIN PhD student

Danny Boerrigter

DANNY BOERRIGTER Research assistant

ROXANNE CADIZ Technical assistant

YIRU ZHANG PhD student

KATE NAUDE Research assistant

Juan Olaya

JUAN OLAYA PhD student

DR MARI KONDO Postdoctoral Fellow

HELEN CAI PhD student

PUBLICATIONS

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.