A Puzzle Worth Finishing
Updated: May 19, 2021
We are currently witnessing a global action to drive innovation in Alzheimer’s disease.
The pervasiveness of Alzheimer’s disease (AD) in our global society is tangible. AD affects 50 million people worldwide with nearly 10 million new cases every year. Someone develops dementia every 3 seconds. As abnormal proteins called amyloid and tau, pernicious deposits that form plaques and tangles, accumulate in a person’s brain causing it to shrink over time, they may start to forget, get confused, or have difficulty learning new things. The grim reality is that despite the success of scientific advancements in drug and non-drug options to mitigate the progression, there is still no cure for this progressive degenerative disease. Bill Gates equated fighting against AD to completing a puzzle: “Your goal is to see the whole picture, so that you can understand the disease well enough to better diagnose and treat it. To see the complete picture, you need to figure out how all of the pieces fit together.”
Contrary to popular belief, not all individuals with AD have amnesia (loss of memory).
One piece of the puzzle is clinical heterogeneity of AD. From its initial inception in 1906 to present, research has shown that AD profiles can be diverse with some presenting with memory troubles at a late age of onset, while others exhibiting various cognitive deficits at a younger age. Contrary to popular belief, not all individuals with AD have amnesia (loss of memory). In the absence or relative preservation of memory functions, individuals with atypical forms of AD may present with a primary language, visual, or executive functioning impairment. To further distinguish from the typical amnestic cases, research approximates 5–10% of AD cases to be that of early-onset, where individuals develop symptoms before the age of 65—in some cases in their 30s or 40s.
Neuroscience is also making parallel headway. Cutting-edge brain imaging techniques not only show the patterns of brain shrinkage and activity across AD subtypes, but also amyloid and tau burden in the brain. Molecular markers like cerebrospinal fluid and amyloid and tau scans likewise contribute to an accurate diagnosis of AD, leading to more treatment options including clinical trials and cognitive rehabilitation therapies. What’s next on the horizon? A simple blood test to detect AD and clinical trials of immunotherapy are only a few of many exciting developments underway! We are currently witnessing a global action to drive innovation in AD. The fight against AD is not an easy puzzle to finish, but definitely one worth fighting for.
Shalom (Shaz) Henderson [2020, Clare College] is a PhD student at the MRC Cognition and Brain Sciences Unit. She is also a speech-language pathologist by background.