Alzheimer's disease is the leading cause of dementia, characterized by a gradual decline in cognitive functions, including memory, reasoning, and the ability to perform daily tasks. It is linked to the accumulation of amyloid-beta plaques and tau protein tangles in the brain, leading to neuronal damage. Although the disease develops over several decades, early interventions that target metabolic and vascular health offer potential for prevention.
Several modifiable factors influence the risk of developing Alzheimer's disease by affecting brain and general health.
Reduces levels of brain-derived neurotrophic factor (BDNF), which is essential for neuronal health.
Disrupted sleep compromises the elimination of amyloid-beta plaques by the glymphatic system.
Associated with a reduction in glucose metabolism in the brain and an increased risk of neurodegeneration.
Diets high in processed foods increase oxidative stress and inflammation, both of which contribute to Alzheimer's disease.
Symptoms develop gradually, from mild cognitive impairment (MCI) to severe dementia.
Advances in imaging and biomarker testing allow for earlier and more accurate detection of Alzheimer's disease.
Detect amyloid-beta plaques in the brain
Measure levels of amyloid and tau proteins in cerebrospinal fluid.
Standardized tests to assess memory, reasoning, and language skills.
Identifies genetic predisposition; APOE e4 significantly increases risk.
Treatment focuses on managing symptoms, slowing disease progression, and improving quality of life.
Cholinesterase inhibitors: Slow down the degradation of acetylcholine, supporting communication between neurons.
NMDA receptor antagonists: Help regulate glutamate levels to protect neurons.
Regular exercise improves vascular health and reduces oxidative stress.
Cognitive training to maintain brain functions.
Trials that target the early elimination of amyloid-beta plaques prior to the accumulation of tau proteins.