Takako Niikura

Assistant Professor

Biography: 

Dr. Takako Niikura joined the Faculty of Health Sciences at Simon Fraser University as an Assistant Professor in 2009. Dr. Niikura finished the Veterinary School at Hokkaido University in Japan, took an industrial job for a few years, and then, started her research career in basic science at NERC Institute of Virology and Environmental Microbiology (currently Centre for Ecology & Hydrology, Oxford, UK).

She then move to the U.S. and worked at Thomas Jefferson University School of Medicine (Philadelphia, PA) and Michigan State University Department of Biochemistry (East Lansing, MI) as a research associate. In 1997, Dr. Niikura moved back to Japan and started projects in neurodegenerative disorders at Keio University School of Medicine (Tokyo). Dr. Niikura, with her team, studied mechanisms of neuronal death underlying Alzheimer’s disease pathogenesis using in vitro system and discovered a novel 24-residue peptide, Humanin (HN).

In 2007, Dr Niikura took an assistant professor position at Georgetown University School of Medicine (Washington, DC) and was involved in translational research of Alzheimer’s disease including the efficacy testing of Humanin.

More information about the Niikura Lab

Research Interests: 

Research in my laboratory is focused on molecular mechanisms of the age-related neurodegenerative disorders, particularly Alzheimer’s disease (AD) and Amyotrophic lateral sclerosis (ALS).

AD is the most common form of dementia. More than 95% of AD cases are sporadic and the cause(s) of sporadic AD are still unknown except that aging is a risk factor. It is assumed that age-related physiological changes contribute to the initiation and progression of AD. Currently approved drugs for AD are symptomatic; they enhance cognitive function and improve quality of daily life. However, they do not stop the disease progression. To reduce the AD-related impact both on the patients and the societies, additional therapeutic options are desired.
I have been working on a neuroprotective factor, Humanin (HN), as a therapeutic candidate for AD. HN, a 24-residue peptide, is a multi-functional factor with neuroprotective activity against AD-related cytotoxicities. HN suppresses neuronal death caused by all AD-related insults so far tested in vitro including cytotoxic amyloid beta. A highly potent HN derivative ameliorated amnesia in AD mouse models. The action mechanism of HN at the molecular level is currently under investigation.

In addition to investigation related to AD, I have extended my research interest to ALS, a motor neuron disorder. Superoxide dismutase 1 (SOD1) and ALS2 are responsible genes for familial ALS. Using these mutant genes as model, I have been investigating molecular mechanisms of motoneuronal death underlying ALS.

Publications and Activities