International Graduate School of Neuroscience

What can transgenic mouse models tell us about the pathogenesis of Alzheimer’s disease?

Friday, September 25, 2015, 11 a.m., Seminar Room FNO - 01 / 117

• Heikki Tanila
• Department of Neurobiology,A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio

Alzheimer's disease (AD) is typically a slowly progressing neurodegenerative disease of the elderly. By the time the affected individual has reached the end stage of the disease, and the brain will be subject for post-mortem analysis, it has born years of various pathological processes. Therefore what we see at autopsy of AD patients tells little about the most critical early stages of the disease process. Transgenic mouse models offer a unique possibility to observe putative disease processes from the very beginning. All current genetic AD mouse models carry one or several of the known gene mutations that account for the rare early-onset AD. Mice carrying mutated amyloid precursor protein (APP) alone or in combination with presenilin-1 (PS1) mutation develop similar amyloid plaques as found in the human brain and show similar inflammatory response around the plaques as humans. In contrast, mice carrying tau mutations linked with familial fronto-temporal dementia develop aggregates of hyperphosphorylated tau, but seldom true neurofibrillary tangles as found in the AD brain. Both amyloid and tau transgenic mice display memory impairment as they age. There are also mouse model carrying all the above mentioned transgenes. However, it is questionable whether we can claim that there is a mouse model of AD. Rather, we have a sophisticated 'toolkit' of mouse models for various pathological processes

Host

• Denise Manahan-Vaughan
  Department of Neurophysiology, Faculty of Medicine, Ruhr-University Bochum