Alzheimer’s disease (AD) is a common neurodegenerative disorder causing progressive memory loss and cognitive dysfunction. The amyloid-β precursor protein (APP), which has an unknown role in the brain, has long been suspected to be at the heart of AD. In the brain, APP is broken down into a smaller molecule called amyloid-β. Visible clumps, or plaques, of amyloid-β found in the autopsied brains of patients are a hallmark of Alzheimer’s, but scientists have long debated whether the plaques are a cause of the neurodegenerative condition or a consequence of other biochemical changes associated with the disease. The cortex and hippocampus, two major brain regions that develop amyloid plaques and neurofibrillary tangles in AD, are the brain regions crucial for cognition. Current AD therapies mainly target proteins to modulate one specific type of neurons, the cholinergic neurons. However, neurodegeneration associated to AD is not limited to a specific neurotransmitter system such as acetyl choline, and other systems, including those related to dopamine and histamine are also deregulated in AD. Our hypothesis is that some of these neurotransmitter systems can be novel targets to protect against disease progression and or protect against the aberrant signaling that occurs upon plaque formation.