This document discusses antidepressant and anti-dementia drugs. It notes that depression is a mood disorder and major cause of disability worldwide, and can lead to suicide. It describes how selective serotonin reuptake inhibitors (SSRIs) like Prozac and Zoloft work to treat depression by increasing serotonin levels in the brain. It also mentions tricyclic antidepressants from the 1970s and monoamine oxidase inhibitors (MAOIs) as older classes of antidepressants. The document provides references on antidepressant mechanisms of action, neuroinflammation, and treatment-resistant schizophrenia.
This document discusses antidepressant and anti-dementia drugs. It notes that depression is a mood disorder and major cause of disability worldwide, and can lead to suicide. It describes how selective serotonin reuptake inhibitors (SSRIs) like Prozac and Zoloft work to treat depression by increasing serotonin levels in the brain. It also mentions tricyclic antidepressants from the 1970s and monoamine oxidase inhibitors (MAOIs) as older classes of antidepressants. The document provides references on antidepressant mechanisms of action, neuroinflammation, and treatment-resistant schizophrenia.
This document discusses antidepressant and anti-dementia drugs. It notes that depression is a mood disorder and major cause of disability worldwide, and can lead to suicide. It describes how selective serotonin reuptake inhibitors (SSRIs) like Prozac and Zoloft work to treat depression by increasing serotonin levels in the brain. It also mentions tricyclic antidepressants from the 1970s and monoamine oxidase inhibitors (MAOIs) as older classes of antidepressants. The document provides references on antidepressant mechanisms of action, neuroinflammation, and treatment-resistant schizophrenia.
This document discusses antidepressant and anti-dementia drugs. It notes that depression is a mood disorder and major cause of disability worldwide, and can lead to suicide. It describes how selective serotonin reuptake inhibitors (SSRIs) like Prozac and Zoloft work to treat depression by increasing serotonin levels in the brain. It also mentions tricyclic antidepressants from the 1970s and monoamine oxidase inhibitors (MAOIs) as older classes of antidepressants. The document provides references on antidepressant mechanisms of action, neuroinflammation, and treatment-resistant schizophrenia.
Dementia Drugs) Under supervision Prof. Dr. Amany Ali Prepared by Alaa Mohamed Nasr introduction
Depression is disorder of mood
Globally more than 350 million people of all ages suffer from depression Depression is a major cause of disability World wide Depression can lead to suicide MAOIS Mechanism of Action: SSRIs, such as fluoxetine (Prozac) and sertraline (Zoloft), work by increasing the levels of serotonin in the brain. They inhibit the reuptake of serotonin, allowing it to remain active in the synaptic cleft, thereby improving mood and reducing symptoms of depression. Tricyclic Antidepressants (TCAs): 1970 References Effendi, W.I.; Nagano, T.; Kobayashi, K.; Nishimura, Y. Focusing on Adenosine Receptors as a Potential Targeted Therapy in Human Diseases. Cells 2020, 9, 785. [Google Scholar] [CrossRef] [PubMed] Vahid-Ansari, F.; Albert, P.R. Rewiring of the Serotonin System in Major Depression. Front. Psychiatry 2021, 12, 802581. [Google Scholar] [CrossRef] [PubMed] Lu, J.; Huang, C.; Lu, Q.; Lu, X. Therapeutic and Prophylactic Effects of Amphotericin B Liposomes on Chronic Social Defeat Stress-Induced Behavioral Abnormalities in Mice. Front. Pharmacol. 2022, 13, 918177. [Google Scholar] [CrossRef] Buckley, P.F. Neuroinflammation and Schizophrenia. Curr. Psychiatry Rep. 2019, 21, 72. [Google Scholar] [CrossRef] Howland, J.G.; Greenshaw, A.J.; Winship, I.R. Practical Aspects of Animal Models of Psychiatric Disorders. Can. J. Psychiatry 2019, 64, 3–4. [Google Scholar] [CrossRef] Nucifora, F.C., Jr.; Woznica, E.; Lee, B.J.; Cascella, N.; Sawa, A. Treatment resistant schizophrenia: Clinical, biological, and therapeutic perspectives. Neurobiol. Dis. 2018, 131, 104257. [Google Scholar] [CrossRef] [PubMed]