Hello there, BSR readers; it’s good to be back. It’s been a while since I’ve posted anything—that’s because I’ve recently made some pretty big life transitions. After graduating from the Psychology Department last May, I was lucky enough to land a job at Stanford Research International. While I miss being able to protest between classes, and study in trees, and though I often find myself overwhelmed with Silicon Valley preppies, it has been a wonderful experience thus far. I am currently participating in wonderful and novel Alzheimer’s research in Joseph Rogers’s laboratory of the neurobiology of aging. I want to share with you the science that has motivated me.
Before we talk cures, I need to first explain the disease itself. Alzheimer’s disease (AD) is a neurodegenerative disorder that is the sixth-leading cause of death in the United Sates and affects an estimated 5.4 million Americans. AD most often occurs later in life. It is characterized by progressive deterioration of brain function, and ultimately leads to death. On a cellular level, AD is associated with loss of neurons and synaptic connections within the cerebral cortex. AD patients also experience atrophy of many brain regions including the amygdala (which is dedicated to management of basic emotions), the frontal lobe (the part of the brain responsible for logic and behavior regulation), and the hippocampus (which aids memory).
Regardless of the large body of research that has been dedicated to AD, and despite the well-understood neuropathology of this disease, the root cause of this disorder remains obscure. The most widely accepted hypothesis for the cause of AD is the amyloid hypothesis, which postulates that the primary cause stems from deposits of the peptide amyloid beta (Abeta) within the brain. Abeta is a multifunctional protein that facilitates many processes (including kinase activation and regulation of cholesterol transport). However, Abeta is highly elevated in AD patients, causing the protein to form aggregates (called plaques) within the brain. In large enough amounts, these plaques initiate the damage to neurons.
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