Causes of Alzheimer’s disease
The exact trigger of Alzheimer’s disease is unknown. But we do know what happens after the condition is triggered and the process of pathogenesis starts. Apparently, the catalyst of Alzheimer’s disease features genetic predisposition paired with environmental factors that induce a cascade of events ending up in dementia. Thus, instead of causes, we can list a few risk factors:
- Advanced age: Seniors are at a higher risk of Alzheimer’s disease as their age increases. Depending on various risk factors and environmental conditions, patients may start experiencing symptoms sooner or later in their lifetime.
- Family history: As noted above, having family members with Alzheimer’s disease increases the risk of suffering from the same problem. There’s a genetic predisposition to it. Still, it is not the only risk factor, and only carrying a gene is not enough to trigger the disease.
- Obesity: Overweight and obese individuals have a higher rate of Alzheimer’s disease, and exercise has been recognized as a protective factor. In contrast, living a sedentary lifestyle, having high-fat levels in the blood, and experiencing insulin resistance problems increase your risk of Alzheimer’s disease.
- Cardiovascular problems and inflammation: Studies show that chronic inflammation has a role in the pathogenesis of Alzheimer’s disease. High inflammatory markers are a risk factor, especially when combined with hypertension and vascular problems affecting the brain.
- Head trauma: Patients who receive head trauma are at a higher risk of developing the disease. Being diagnosed with a traumatic brain injury predisposes patients to Alzheimer’s disease and other types of dementia.
Regardless of the initial trigger, once Alzheimer’s disease starts, it features the formation of amyloid plaques in different areas of the brain. Amyloid is a protein that apparently has a normal function in the brain, but Alzheimer’s patients have an excess that builds up. As it does, amyloid plaques surround neurons while tangles develop inside nerve cells. Together, plaques and tangles obstruct normal brain function as they accumulate in more areas of the brain. These areas undergo atrophy, and the related cognitive functions deteriorate as the disease progresses.