Alzheimer’s disease (AD) is a progressive and irreversible neurodegenerative disease and is the most common cause of dementia in elders in the industrialized world.

Neuroanatomical changes resulting in AD include accumulation of amyloid-β  and formation of plaques, but how these neuropathologies affect the brain is poorly understood.

Olfactory impairment is an early symptom of AD and is used as a preclinical marker in humans - but is this behavioral symptom also developed by the transgenic AD model mouse strain Tg6799? And if it is, does it precede other behavioral symptoms and how does it correlate to neuropathologic amyloid-β plaque load?

 

1. Evaluate the development of an olfactory impairment in the Tg6799 mice,

2. Determine at which age such an impairment arises.

3. Test whether the mice also develop other behavioral deficits and at which age these impairments arise.

4. Evaluate  the presence of amyloid-β plaques in olfactory brain structures histologically.