Alzheimer’s and other dementias are difficult diseases for individuals to deal with. It seems strange that our Lord takes people home one personal memory at a time, until little is left of the person we knew and loved. Alzheimer’s is also a disease for which there is currently little in the way of a cure or even treatment. It has been a puzzle since Alois Alzheimer first described it in 1907.
Alzheimer’s destroys neurons in the brain that use the neurotransmitter acetylcholine. The first attempts at treatment were medications that boosted the actions of the remaining acetylcholine neurons or acted in the place of this neurotransmitter. Unlike drugs that reduce the symptoms of Parkinson’s disease by augmenting the dopamine system, these medications were mostly ineffective in Alzheimer’s disease. Alois Alzheimer described plaques and tangles in the brains of individuals who had died of this disease, so another attempted strategy was to target the malformed proteins that are responsible for these abnormalities: amyloid-beta and tau. So far, this approach has also not proven to be a useful way to delay or reduce the disease.
One of the reasons treatments have proved so ineffective is that the diagnosis of Alzheimer’s is difficult; currently, the disease can only be confirmed in a post-mortem examination of the brain. Researchers believe that if we had a reliable tool to diagnose this disease earlier, then perhaps some of the treatments would be more effective. However, it is also possible that we do not have a proper understanding of the cause of the disease. Recently, a new suggestion that the brain’s immune system may play a major role in provoking this disorder has received more attention.
In the brain, in addition to neurons, there are other cells called microglia that support the neural system. They function as the resident immune cells of the brain, cleaning up problems such as the debris from cells that die. They are also known to play a role in the neural changes involved in learning and memory. A recent finding is that microglia may have an important role in animal models of Alzheimer’s. There are strains of mice that develop Alzheimer-type dementia. When the functioning of the microglia in these mice is changed by modifying a key inflammation gene in these cells, the dementia is prevented. The exact role of this gene and how it prevents the memory decay is not yet clear, however.
Other evidence linking microglia to Alzheimer’s arises from studies that have looked for genes predisposing individuals to Alzheimer’s. The function of these risk genes appears to be microglia-specific. One function of the microglia is to clear amyloid-beta plaques, but in doing this clearance, they may also release proteins that could “seed” new plaques, making the disorder worse. Based on this apparent relationship between Alzheimer’s and microglia, at some stages of the disease the actions of microglia may need to be turned up or down, and this direction may change as the disease progresses.
What is important about this work is both that it gives us another way to understand how Alzheimer’s develops and that it suggests alternate routes to attack the disease. We are still far away from possible human treatments, and they may be complex, but there is excitement in the scientific community that we are on the verge of a new day in dealing with this debilitating and painful disorder. Research on dementia has seen little progress for many years, so please join me in praying for and supporting the science that may lead to a way out of the brokenness in creation that is Alzheimer’s.
You just read something for free.
But it didn’t appear out of thin air. Writers, editors and designers at Christian Courier worked behind the scenes to bring hope-filled, faith-based journalism to you.
As an independent publication, we simply cannot produce award-winning, Christ-centred material without support from readers like you. And we are truly grateful for any amount you can give!
CC is a registered charity, which is good news for you! Every contribution ($10+) is tax-deductible.