Alzheimer’s disease (AD) is a progressive neurologic disorder that causes the brain to shrink (atrophy) and brain cells to die. It is the most common cause of dementia, which leads to cognitive function deterioration. Globally, 50 million people are affected by dementia, and between 60-70% are estimated to have AD. The exact cause of AD is not yet fully understood, but factors like aging, family history, untreated depression and lifestyle factors associated with cardiovascular disease are thought to increase the risk of developing AD.

In AD, many neurons stop functioning, lose connections with other neurons, because proteins build up and form abnormal protein aggregates called ‘plaques’ and ‘tangles’. Eventually, nerve cells die, and brain tissue is lost. As AD is a progressive disease, which means gradually, more parts of the brain are damaged resulting increase or worsening of symptoms. At early stage of disease develops, the first sign is usually minor memory problems such forgetting about recent activities. However, as the disease progresses, memory problems become severe, and other symptoms may also be present.

Currently, medications may temporarily improve or slow the progression of symptoms. These treatments can sometimes help people with AD maximize function and maintain independence for a period of time. As there are no treatments that cure AD or alter the disease progression in the brain, the demand for novel therapeutics remains high. The use of Aan I-EEG drug screening platform can facilitate and expedite drug discovery to address this unmet medical need.

Animal Models for Alzheimer’s Disease

Transgenic AD models mimic a range of AD-related pathologies. They have greatly contributed to the advancement of AD research, allowing us to study gene function and evaluate potential therapeutic strategies in the disease progression.

Double Transgenic Mouse Model

The double transgenic mouse model (APPswe/PS1dE9) of AD has been widely used in experimental studies. APP/PS1 are double transgenic mice expressing a chimeric mouse/human amyloid precursor protein and a mutant human presenilin 1, targeting neurons of the central nervous system. Both mutations are associated with early-onset AD. This model’s behaviour mimics behavioural changes in early-stage human AD patients, making it a suitable animal disease model for novel drug discovery.

Triple Transgenic Mouse Model

The triple transgenic mouse model (3xTg-AD) harbours the human amyloid precursor protein, presenilin knock-in mutation, and tau P301L mutant transgene. 3xTg-AD mice exhibit striking aberrations in oligodendrocyte marker expression and myelin ultrastructure abnormalities as compared to age-matched control mice.