What Causes Alzheimer's Disease and How Does It Develop?
Normal cell functions generate free radicals. They are by-products of biochemical reactions, such as converting the food we eat into the form of energy cells can use. When we are healthy, our bodies naturally maintain a balance between antioxidants and free radicals. (iv.1, 5, 52, 53)
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Over time, chronic disease conditions can upset this balance. Diseases and conditions that increase the risk of Alzheimer's include: (iv.1, 5, 39, 52, 53)
Traumatic brain injury (e.g., concussions) and heavy metal toxins (e.g., lead, iron, and aluminum) can also overwhelm our immune system's ability to heal and restore balance. Unregulated inflammation and cell damage can then lead to neurodegenerative disorders as well as learning and memory disabilities. (iv.1, 5, 39, 52, 53)
What Are Brain Plaques?
Evidence indicates free radical damage and inflammation can produce potentially toxic proteins called amyloid-β and abnormal tau. When the innate immune system fails to clear out these proteins and their peptide fragments, they accumulate over the years. Clumped together, these proteins form the amyloid plaques and tangled fibrils in the brain characteristic of Alzheimer's disease. Studies suggest they have deadly effects on neuron brain cells: (iv.1, 5, 52, 53)
Events Leading to Alzheimer's Disease
Damage to Neurons and Lower Levels of an Essential Neurotransmitter
The toxic effects of amyloid-beta (Aβ) plaques are found to be most severe from the basal forebrain through the cerebral cortex region of the brain. (iv.54, 55)
The Brain
Alzheimer's disease causes damage to and loss of large numbers of neuron brain cells that produce acetylcholine (ACh). This leads to lower levels of ACh in the brains of patients with Alzheimer's disease. ACh is an essential brain chemical for learning and memory. Loss of ACh is directly linked to symptoms of dementia in Alzheimer's. (iv.54, 55)
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