Which type of elder mistreatment is demonstrated by a caregiver leaving a nursing home resident alone in his room for long periods at a time with no opportunity for social stimulation?

A. Dopamine is primarily associated with other neurodegenerative disorders such as Parkinson's disease, not Alzheimer's disease. In Alzheimer's disease, the focus is on changes related to beta-amyloid plaques and neurofibrillary tangles rather than alterations in dopamine levels.
B. Glial cells, including astrocytes and microglia, play a role in the brain's immune response and support of neurons. In Alzheimer's disease, there is evidence of increased activation and proliferation of glial cells in response to neuroinflammation and the presence of beta-amyloid plaques and neurofibrillary tangles. This reactive gliosis is a secondary response to the underlying pathology.
C. Glutamate is an excitatory neurotransmitter involved in various brain functions, including memory and learning. In Alzheimer's disease, there is evidence of dysregulation in glutamate metabolism and

signaling pathways. This dysregulation can lead to excitotoxicity, which contributes to neuronal damage and cell death seen in the disease.
D. Neurofibrillary tangles are one of the hallmark pathological features of Alzheimer's disease. These tangles are aggregates of hyperphosphorylated tau protein that accumulate inside neurons, disrupting their normal functioning and eventually leading to cell death. Neurofibrillary tangles, along with beta- amyloid plaques, contribute to the progressive cognitive decline observed in Alzheimer's disease.

A. ALS is not caused by a virus or inflammation of the nerves. It is a progressive neurodegenerative disease affecting the motor neurons in the brain and spinal cord.
B. While acetylcholine breakdown is involved in other neurological conditions (such as myasthenia gravis), ALS primarily affects motor neurons and does not directly involve acetylcholine metabolism at the neuromuscular junction.
C. ALS does not typically involve significant inflammation or demyelination (which is more characteristic of conditions like multiple sclerosis). Therefore, reducing CNS inflammation is not a therapeutic target in ALS.
D. Riluzole, the medication prescribed for ALS, works by decreasing the release of glutamate, which is a neurotransmitter that can be toxic to nerve cells in high amounts. In ALS, excessive glutamate release is believed to contribute to motor neuron degeneration. By reducing glutamate release, riluzole may help protect motor neurons and slow the progression of the disease.