“What causes Alzheimer’s disease” and “How does the brain work” should not be seen as two different questions because if Alzheimer’s disease affects how the brain works, exploring new answers about brain functions could become meaningful in delaying, preventing or mitigating Alzheimer’s disease.
Amyloid and tau proteins in Alzheimer’s disease
In a Diseases & Conditions entry, Alzheimer’s Disease, by Cleveland Clinic, they wrote, “An abnormal build-up of proteins in your brain causes Alzheimer’s disease. Specifically, two proteins called amyloid and tau. Your brain has billions of nerve cells called neurons. Your neurons let you think, learn, remember and plan. Amyloid protein sticks together in your brain cells, forming clumps called plaques. Tau proteins twist together in fiber-like strands called tangles.”
“These plaques and tangles prevent neurons from working as they should. They block neurons’ ability to send electrical and chemical signals back and forth. When amyloid and tau proteins build up in your brain, they slowly kill neurons. This causes permanent damage that leads to Alzheimer’s symptoms. Nerve cell death starts in one area of your brain and then spreads to other areas. It’s most common for Alzheimer’s to begin in the area of your brain that controls memory — your hippocampus.”
Neurons
The necessity for how the brain works, for example, is to seek out how “neurons let you think, learn, remember and plan”. If neurons are doing these, how so? What part of neurons allows for thinking? What part of neurons ensures that learning something is possible and to have that in memory? How do neurons determine remembering? What makes neurons responsible for planning in a way that allows details?
The reason for these questions is because the anatomy and physiology of neurons are quite established in brain science. What parts of neurons are correlated with those functions? If the answer is that neurons are in clusters, then what makes the cluster for planning different from the cluster for learning or remembering?
Synapses
If the answer is the synapse, rather than the cluster, then what is the difference between the synapse for one function from the synapse for another function? Are synapses custom, so that some can plan and others can learn? Or, are all functions possible by the same design of synapses, neurons, and clusters?
What else?
What else are the options in the brain for “thinking, learning, remembering and planning” if neurons, synapses, or clusters would be ruled out? Could genes be responsible or glia? How do genes shape specific plans about a trip? Or, how would glia be directly responsible for remembering or memory?
What else? Cleveland Clinic noted, “The plaques and tangles prevent neurons from working as they should. They block neurons’ ability to send electrical and chemical signals.” If electrical and chemical signals are in motion during thinking, learning, remembering and planning, does that not indicate that the focal point for functions should be electrical and chemical signals, rather than to assume them as what neurons send?
For example, to think, remember or plan means that the memory was already stored, and then relayed. So, in what form was it stored, and how was it relayed?
Electrical and chemical signals in Alzheimer’s disease
It can be theorized that electrical and chemical signals are the basis for information organization and relay, such that they are responsible for functions and how those functions are graded. This conceptually means that in clusters of neurons, electrical and chemical signals are in sets. It is within these sets that they hold specific configuration or formation for information, say of a memory, a feeling or an emotion. It is also from these sets that summaries are provided to be relayed to other sets.
It is possible to explore electrical and chemical signals for how they mechanize functions and use that to seek how Alzheimer’s disease might be better understood towards prevention, delay or mitigation. This is also necessary because of the controversy in the Alzheimer’s disease research community.
The amyloid hypothesis in Alzheimer’s disease
There is a recent guest essay in The NYTimes, The Devastating Legacy of Lies in Alzheimer’s Science, stating that, “For decades, Alzheimer’s research has been shaped by the dominance of a single theory, the amyloid hypothesis. It holds that amyloid proteins prompt a cascade of biochemical changes in the brain that cause dementia. The supremacy of that hypothesis has exerted enormous pressure toward scientific conformity. Even many of the most hardened skeptics of the hypothesis believe that amyloids have some association with the disease.’
“But since the early 2000s, doctors, patients and their loved ones have endured decades of therapeutic failures stemming from it, despite billions of dollars spent in grants and investments. Its contradictions — such as the presence of massive amyloid deposits found in the brains of deceased people who had no symptoms of Alzheimer’s — have long exasperated critics and prompted doubts among many supporters. Still, the hypothesis retains enormous influence. Nearly every drug approved for Alzheimer’s dementia symptoms is based on it, despite producing meager results.”
“The anti-amyloid antibody drugs approved in the United States cost tens of thousands of dollars per patient per year, yet they slow cognitive decline so minutely that many doctors call the benefits imperceptible. The entrenchment of the amyloid hypothesis has fostered a kind of groupthink where grants, corporate riches, career advancement and professional reputations often depend on a central idea largely accepted by institutional authorities on faith. It’s unsurprising, then, that most of the fraudulent or questionable papers uncovered during my reporting have involved aspects of the amyloid hypothesis. It’s easier to publish dubious science that aligns with conventional wisdom.”
This article was written for WHN by David Stephen who currently does research in conceptual brain science with focus on the electrical and chemical signals for how they mechanize the human mind with implications for mental health, disorders, neurotechnology, consciousness, learning, artificial intelligence and nurture. He was a visiting scholar in medical entomology at the University of Illinois at Urbana Champaign, IL. He did computer vision research at Rovira i Virgili University, Tarragona.
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References/Sources/Materials provided by: https://my.clevelandclinic.org/health/diseases/9164-alzheimers-disease
https://sedona.biz/nih-brain-initiative-how-does-the-mind-regulate-the-body/
https://workdrive.zohopublic.com/writer/published/l9e6eb63ac839462f452cb8cab42d425ffca9
https://www.nytimes.com/2025/01/24/opinion/alzheimers-fraud-cure.html
