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If you like to watch thrillers or television detective shows, you can probably picture a typical crime scene—furniture turned over, clothes strewn everywhere, perhaps a weapon, blood splatter, and yes, a body or two. As crime scene investigators photograph the scene, collect fingerprints, and carefully package evidence, the lead detective steps past the yellow tape, surveys the room, and identifies the critical clues that ultimately lead to the perpetrators' capture.

If only disease scene investigations were as straightforward as a Hollywood crime scene, it would make stopping a disease in its tracks so much easier. In some ways, examining the brain of a person who died with Alzheimer’s disease is like looking at a crime scene—dead brain cells everywhere, missing nerve synapses, nefarious protein deposits, smoldering inflammation—with one big difference: the crime transpired over 10 years ago. For a scene like this, altered by time and the elements, it would be virtually impossible to identify the culprit.

Despite hundreds of millions spent on research by the smartest minds in science and medicine, the precise cause of Alzheimer’s disease remains a mystery.

If there is one telltale clue that binds the most common forms of dementia, it would be the accumulation of abnormal proteins—for Alzheimer’s disease, it’s amyloid-beta and tau proteins; for Lewy body dementia, it’s alpha-synuclein; and for frontotemporal dementia, it’s TDP-43. These peculiar proteins are the smoking guns of dementia. It has long been known that these proteins accumulate in the brains of people who suffer from dementia, but what nobody knows is whether they’re the actual cause or merely the effect of the mysterious processes that lead to the progressive forgetfulness and........

© Psychology Today