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CASE 9: ALZHEIMER'S DISEASE

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> CASE 9 Alzheimer's Disease

Norma B. was shocked when the doctor gave her the diagnosis of mild, late onset Alzheimer's disease (AD) at age 91. Her husband Georg was not; it explained her increasingly strange behavior over the past few years. She had been ever more dependent on him for names and details of events, repeating the same information several times in a short period, misplacing kitchen and other items, and losing hundreds of dollars.

They phoned each of their grown children to share the sad news. They were determined that this would not change their lives. In fact, Georg became more patient now that he understood Norma's behavior. Georg and Norma had only just found each other again, college sweethearts reunited in their 70s after a lifetime apart. Norma admitted to her daughter the early difficulties: “It's really hard because I’m losing my friendships.” She told her, “I feel lonely; I can’t talk to them because I forget the words. They are so kind and make an effort to include me, but I’m ashamed. It's embarrassing.”

Late-onset Alzheimer's disease, the most common form, begins with age-related free radicals, generated in the mitochondria, cause oxidative stress which further damages the mitochondria, disrupting ATP production. With loss of ATP to fuel maintenance of the membrane resting potential, the disrupted mitochondrial cell membrane becomes permeable to an influx of damaging levels of calcium while leaking large proteins into the surrounding cell. Leaked proteins are neurotoxic and produce senile plaques and neurofibrillary tangles, two pathological findings in AD. Senile plaques are extracellular deposition of beta amyloid-Aβ, causing neuron death, synapse damage, and loss of long-term potentiation. New diffusion tensor imaging to view white matter axon tracts reveals selective early degeneration within the limbic–diencephalic network. This causes early disruption in memory, behavior, and emotion due, in part, to loss of acetylcholinergic cells. MRI imaging shows selective early damage from plaques to the entorhinal cortex and hippocampus, disrupting path-finding directionality (such as whether to turn left or right) and memory loss. Secondary damage from intracellular accumulation of tau protein disrupts axon transport and is found extracellularly in neurofibrillary tangles. Abnormal tau first appears in the entorhinal cortex, then in the hippocampus, and at later stages in the association cortex.

Norma's clinical findings were consistent with the early damage to the limbic system pathways involving memory, behavior, and emotions. Her symptoms progressed very slowly over the next few years. She was the choir director at their church, and when this became too difficult to manage, she cut back to just playing the piano during service, which remained easy due to years of practice. However, she noticed that she would forget the song order and constantly have to check the printed schedule, something that had never happened before. She became focused on earlier events in her own life as recent memory faded; she replaced the photos of her grandchildren with a photo of her own grandfather. ...

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