Question

A male in his 80s was referred for an evaluation. He had previously been diagnosed with Alzheimer’s dementia. At the time of evaluation, he was living at home with assistance from his family and caregiver. He is now unable to learn most any new information, and long-term memories are also weak (sometimes forgetting who his wife and children are). He is sometimes hard to understand
due to slurring of words, and he appears to see people who are not in the room. He is needing help in bathing, dressing, cutting his own food and using of toilet. Due to falls, he is usually transported via wheelchair.

During the evaluation, he was unable to state his age, the current month, the current year, and the city where he’s located. He can read a list of 3 words but could not remember any of them after just 1 minute.

Cholinesterase inhibitors and Memantine are administered. His family noted that they are struggling to provide care to him, and they asked whether it would be appropriate to consider moving him to a residence with a memory care unit.

1. Make a pathophysiology of the disease based on the case scenario.

Answer 1

alzheimer disease is characterized by loss of neurons and synapes in brain cortex and certain subcortical regions . This loss results in gross atrophy of affected region , including degeneration in temporal lobe and parietal lobe and parts of frontal cortex and cingulated gyrus . Neurons have tubular support structure made of microtubules , protein which help in its stability is tau protein. In Alzheimer's disease due to etiological factors such as aging , toxic chemicals , environmental stress -- tau protein changes occur causing microtubules to collapse and tau protein clumps together to form neurfibrillary tangles and also extracellular deposition of beta amyloid plaques occurs due to which granulovascular degeneration thus causing loss of cholinergic nerve cells ( which is important for memory) , thus leading to memory loss; damage in function of temporal , parietal and frontal lobe and in cognition . Gross pathophysiological changes which can be seen due to it are shrinkage of cerebral cortex , cortical atrophy , enlarged ventricles , basal ganglia wasting and shrinking of hippocampus. Microscopically can be seen are changes in protein of nerve cell of cortex , amyloid plaque accumulation and neurfibrillary tangles accumulation , granovascular degeneration and loss of cholinergic nerve cells .

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