Researchers suspect that Alzheimer’s disease (AD) might be caused by the same mechanism that helps a healthy mind from being mired by minutia–like remembering what you ate for lunch for the past 8 Tuesdays–but for Alzheimer’s patients the mechanism has gone into overdrive and with it stuck in reverse.

In a normal brain there is a continual process where amyloid precursor protein (APP) is attacked, by the protein caspases, and broken down. Researchers had previously demonstrated the key role this process plays in Alzheimer’s by preventing it to take place in mice genetically engineered with the human Alzheimer’s gene. With the process prevented the mice did not develop Alzheimer’s.

Dale Bredesen, MD, Buck Institute, believes that memories are made and broken by the process of caspases breaking down amyloid precursor protein, which is why young brains are more adept to making and breaking memories. The problem with Alzheimer’s diseased brains is that they become better at breaking memories rather than making them.

As expected when they compared Alzheimer’s patients, to people of the same age, there was a greater amount of A-beta, which is the result of APP being broken down. What surprised the researchers is that younger people had up to 10 times the amount of the protein being broken down as Alzheimer patients.

Researchers now realize that A-beta is produced in the brain throughout life and it is a regulator of the synapses–the connections between neurons–and not a direct cause of Alzheimer’s. Many people develop A-beta plaques without developing symptoms of Alzheimer’s. The researchers suspect that because many people develop A-beta without developing symptoms of Alzheimer’s that it is not A-beta itself, but a signal being sent downstream that triggers the development of the disease.

Scientist are now looking for the ‘downstream’ pathways and ways to therapeutically target them. Their efforts are to restore balance and to disconnect the molecular mechanism that throws memory-making into reverse.