Researchers recently found that a common antidepressant, citalopram, reduces levels of a protein associated with Alzheimer's disease. There tend to be higher levels of the protein amyloid beta in Alzheimer's patients. The excess proteins clump together and form plaques in the brain. The neurotransmitter serotonin reduces levels of amyloid beta. Because many antidepressants help to maintain serotonin circulation in the brain, researchers wondered if they could help lower levels of the plaque causing protein and therefor slow Alzheimer's onset. To test their hypotheses, researchers gave several different antidepressants to mice that had been genetically engineered to develop Alzheimer's disease. When the mice received the antidepressants they had not yet started to develop plaques, but the hope was that the antidepressant would slow or prevent plaque development. Indeed, the antidepressants lowered amyloid beta production by 25 percent after a single day.
In a different experiment researchers gave the antidepressant citalopram to mice that had already developed plaques. Researchers monitored plaque growth in the mice for 28 days after giving them citalopram. Preexisting plaques stopped growing and the rate of new plaque growth lowered by 78 percent, giving the researchers hope that citalopram could treat Alzheimer's in humans.
Researchers, in a separate experiment, gave citalopram to 23 adults between the ages of 18 and 50 who were not suffering from cognitive impairment. Patients who had taken citalopram showed a 37 percent drop in the amount amyloid beta in their spinal fluid. So far it is not recommended that patients take antidepressants solely for the purpose of slowing Alzheimer's onset, but researchers will be further exploring the science behind serotonin's effect on amyloid beta.
Researchers, in a separate experiment, gave citalopram to 23 adults between the ages of 18 and 50 who were not suffering from cognitive impairment. Patients who had taken citalopram showed a 37 percent drop in the amount amyloid beta in their spinal fluid. So far it is not recommended that patients take antidepressants solely for the purpose of slowing Alzheimer's onset, but researchers will be further exploring the science behind serotonin's effect on amyloid beta.
Connection:
This article relates to our study of disease and the nervous system. We learned about homeostatic imbalances and how a homeostatic imbalance is caused by a disruption between structure and function. This article mentions plaque building up in the brain of Alzheimer's patients, while Alzheimer's disease is not fully understood there is a potential disruption. If plaque builds up in the brain and disrupts the flow of information from body to brain or interferes with the function of a certain part of the brain, then the function of the brain is being impaired due to plaque intruding the structure.
In chapter 28 of our text book we read about the nervous system. We learned about the brain and the function of neuron as well as the different divisions of the nervous system. Alzheimer's disease, the disease which centers this article, is a disease of the nervous system. We also learned about neurotransmitters, such as serotonin, the neurotransmitter mentioned in this article. In chapter 28 we learned about how neurotransmitters are sent from the axon terminals of one neuron to the dendrites of another and how they are chemical signals.
Date: May 14, 2014
Author: Michael C. Purdy
Link: http://www.sciencedaily.com/releases/2014/05/140514142326.htm
This article relates to our study of disease and the nervous system. We learned about homeostatic imbalances and how a homeostatic imbalance is caused by a disruption between structure and function. This article mentions plaque building up in the brain of Alzheimer's patients, while Alzheimer's disease is not fully understood there is a potential disruption. If plaque builds up in the brain and disrupts the flow of information from body to brain or interferes with the function of a certain part of the brain, then the function of the brain is being impaired due to plaque intruding the structure.
In chapter 28 of our text book we read about the nervous system. We learned about the brain and the function of neuron as well as the different divisions of the nervous system. Alzheimer's disease, the disease which centers this article, is a disease of the nervous system. We also learned about neurotransmitters, such as serotonin, the neurotransmitter mentioned in this article. In chapter 28 we learned about how neurotransmitters are sent from the axon terminals of one neuron to the dendrites of another and how they are chemical signals.
Date: May 14, 2014
Author: Michael C. Purdy
Link: http://www.sciencedaily.com/releases/2014/05/140514142326.htm
How is this antidepressant taken into the body? By pill, injection, ect?
ReplyDeleteCaroline, to answer your question, Citalopram is generally taken orally in the form of a pill.
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