Alzheimer’s Disease is a progressive neurodegenerative disorder characterized by cognitive decline, memory loss, and behavioral changes. From an endocrinological perspective, this pathology is increasingly linked to dysregulation of glucose metabolism and insulin signaling within the central nervous system, often referred to as ‘Type 3 Diabetes.’ This condition involves the formation of extracellular amyloid-beta plaques and intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein. The resulting neuronal damage and synaptic loss profoundly disrupt communication pathways essential for memory and executive function.
Origin
The disease is named after the German psychiatrist and neuropathologist Alois Alzheimer, who first described the clinical and pathological findings in 1906. This clinical term is rooted in the history of neuroscience and pathological observation of specific brain lesions. Its classification as a distinct neurological disorder arose from post-mortem examination of the brain tissue of a patient experiencing severe dementia.
Mechanism
Pathological mechanisms involve a complex interplay of hormonal and inflammatory factors that drive amyloid and tau deposition. Insulin resistance in the brain impairs energy utilization, directly compromising neuronal health and survival. Chronic systemic inflammation and oxidative stress contribute significantly to the neurotoxic environment. Furthermore, alterations in sex steroid hormones, such as estrogen and testosterone, are implicated in modulating risk and disease progression by influencing brain plasticity and amyloid clearance pathways.
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