CNS & Neurological Disorders - Drug Targets (Formerly Current Drug Targets - CNS & Neurological Disorders) - Volume 13, Issue 6, 2014

Depression is the most prevalent psychiatric disorder (16.6%) and is frequently associated with impairments in several areas. Sexual dysfunction (SD) is a prevalent problem with rates ranging from 40-45% in adult women and 20- 30% in adult men. A relationship between depression and sexual dysfunction has been shown in the literature although the mechanisms of this association are not yet clear. Many antidepressants, especially selective serotonin reuptake inhibitors (SSRIs), list sexual dysfunction as a side effect. New drug alternatives with fewer side effects have been proposed, and bupropion is one of them. This study aims to review the literature on bupropion and its impact in sexual function on depressed subjects. Most of the studies have noted that bupropion is not only as effective as other antidepressants but has the advantage of a lower impact on sexual functioning. Some other studies have found that bupropion can even enhance sexual function in certain individuals. Bupropion is also effective, when combined with other antidepressants, in treating emergent sexual dysfunction. Bupropion may be an alternative treatment for depression that does not include the sexual side effects associated with most of the prescribed antidepressants available; however, additional research is required.

In order to gain insight into the ammonia-detoxification mechanisms in the brain and liver tissues, we have investigated the effects of hyperammonemia in rats, in vivo, on the activity levels of a number of ammonia- and glutamate-metabolizing enzymes in mitochondria and the cytosolic fractions of the cerebral cortex, cerebellum, hippocampus, striatum and liver. In general, the ammonia metabolizing enzymes – glutaminase, glutamine synthetase, glutamate dehydrogenase, AMP deaminase, adenosine deaminase, as well as aspartate aminotransferase and alanine aminotransferase – are differentially upregulated in various brain and liver regions of the hyperammonemic rats, indicating that divergent ammonia-detoxification mechanisms are involved in the various brain regions and liver in acute hyperammonemia.

Melatonin is produced and released by the pineal gland in a circadian rhythm. This neurohormone has proven to be an antioxidant and anti-inflammatory molecule able to reduce or mitigate cell damage associated with oxidative stress and inflammation, and this phenomenon underlies neurodegenerative disorders. These facts have drawn attention to this indole, triggering interest in evaluating its changes and in its relationship to the processes indicated, and analyzing its role in the mechanisms involved at the onset and development of neurodegenerative diseases, as well as its therapeutic potential. Multiple sclerosis, the most common cause of non-traumatic disability in young adults, is a chronic neuroinflammatory disease, characterized by demyelination, inflammation, and neuronal and oxidative damage. In its early diagnosis, it often requires a differential screening with other neurodegenerative diseases with similar symptoms, such as Huntington’s disease, an autosomal dominant disorder. The onset of both diseases occurs in the second or third decade of life. On the other hand, cerebral ischemia is a major cause of human disability all over the world. Although a cerebral stroke can occur as the result of different damaging insults, severe ischemia produces the death of neuronal cells within minutes. Changes in melatonin levels have been observed in these processes (Huntington’s disease, multiple sclerosis and cerebral ischemia) as part of their pathogenic features. This review aims to update and discuss the role played by melatonin during neurodegenerative processes, specifically in multiple sclerosis, Huntington’s disease, and cerebral ischemia, and its possible therapeutic use. We also provide readers with an update on the many neuroprotective mechanisms exerted by this neurohormone in the Central Nervous System.