Question
| A. | Amygdala |
| B. |
Ventral posterolateral nucleus |
| C. |
Nucleus accumbens |
| D. |
Hippocampus |
|
Correct Answer � D Explanation |
|
Answer D) HippocampusShort-term memory loss is often the earliest sign of Alzheimer disease, the most common cause of progressive dementia in the United States.
Hippocampus
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The earliest sites of neurodegeneration in Alzheimer disease are structures in the medial temporal lobe such as the hippocampus and parahippocampal cortex, which are critical for memory formation.
Amygdala
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The amygdala is a structure of the limbic system that plays a role in the processing of emotions.
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Involvement of the amygdala in Alzheimer disease causes emotional lability, depression, and/or anhedonia.
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Damage to a different structure would more likely explain the short-term memory loss in this patient with a normal affect.
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Bilateral damage to the amygdala results in Klüver-Bucy syndrome, which is characterized by emotional lability, anxiety, hypersexuality, hyperorality, and hyperphagia.
Ventral posterolateral nucleus
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The ventral posterolateral nucleus is a structure of the thalamus involved in relaying sensory input from the spinothalamic tract and dorsal column to the primary somatosensory cortex.
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This nucleus does not play a role in memory formation and is not affected in early Alzheimer disease.
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The medial dorsal nucleus of the thalamus and the anterior thalamic nucleus are involved in memory formation.
Nucleus accumbens
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The nucleus accumbens is a basal forebrain structure that has a role in the reward pathway. This structure does not play a major role in semantic (factual) recall.
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Degeneration of other basal forebrain structures such as the nucleus basalis of Meynert can cause memory loss and cognitive decline in Alzheimer disease.
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Decreased GABA secretion by the nucleus accumbens is seen in Huntington disease and anxiety disorders.
