Present Institution:

Universiti Putra Malaysia

Location:

Serdang MY

Career Status:

Faculty Academia
Professor

Bio

Associate Professor Dr. Cheah is an anatomist and the Head of the Department of Human Anatomy. Her expertise spans neuroscience
anatomy
molecular biology
microscopy
and gene therapy. From 2008 to 2020
Dr. Cheah underwent extensive post-doctoral training. Initially
she focused on molecular neurogenetics at the University of Adelaide
Australia
unraveling genes linked to sexual development disorders and neuropsychiatric diseases. Subsequently
she expanded her research into diverse fields
including stroke
cancer biology
and gene therapy at the Massachusetts General Hospital/Harvard Medical School
USA. Active engagement characterizes Dr. Cheah's career
evident through her leadership roles in prestigious organizations like the Malaysian Society of Neurosciences (past Vice-President
MSN)
International Brain Research Organisation-Asia Pacific (past Chair
IBRO-APRC)
Asia Pacific Neurochemistry Society (past Council
APSN)
and International Society of Neurochemistry (council
ISN). She founded the NeuroBiology and Genetics Group at Universiti Putra Malaysia
further establishing her dedication to advancing neuroscience and training talents in the field. For a comprehensive overview of her accomplishments
Dr. Cheah's profile is accessible through her research group's website at: www.neurosains.org.

Interested in presenting:

General Neuroscience
Developmental Neuroscience
Techniques in Neuroscience
Acquiring technical skills
Learning about networking
How to run a lab
Global Networking

Sample of a Science/Scholarship Abstract

1) Global Neuroscience Impact : Funding Opportunities and Partnerships in the Asia Pacific Region 2) AAV mediated gene therapy for rare genetic disorders 3) AAV-mediated Gene Therapy for Neurofibromatosis : Human Perspective & Mouse Model

What type of talks have you presented in the past?

Tuberous sclerosis complex (TSC) arises from the loss of either the TSC1 or TSC2 tumor suppressor gene
encoding hamartin and tuberin
respectively. These proteins form a complex that regulates mTORC1-mediated cell growth. Depletion of either protein results in overgrowth lesions in vital organs. In a mouse model of TSC2
an adeno-associated virus (AAV) vector carrying a condensed form of human tuberin (cTuberin) was utilized for gene therapy. These mice exhibited shortened lifespan and brain pathology akin to TSC. Intravenous injection of AAV9-cTuberin on day 21 extended mean survival and reduced brain pathology
demonstrating the potential of this treatment for life-threatening TSC2 lesions. Conversely
loss of function in the neurofibromatosis type 2 (NF2) tumor suppressor gene leads to schwannomas
meningiomas
and ependymomas
activating the mTOR pathway. Using a novel human schwannoma model in nude mice
direct intratumoral injection of an AAV vector expressing merlin led to tumor regression over 10 weeks. This regression was associated with decreased cell division and increased apoptosis compared to the control group
indicating that merlin re-expression via gene replacement is sufficient for NF2-null schwannoma regression
potentially offering an effective treatment for NF2.