2010
DOI: 10.2147/ndt.s10485
|View full text |Cite
|
Sign up to set email alerts
|

Getting the balance right: Established and emerging therapies for major depressive disorders

Abstract: Major depressive disorder (MDD) is a common and serious illness of our times, associated with monoamine deficiency in the brain. Moreover, increased levels of cortisol, possibly caused by stress, may be related to depression. In the treatment of MDD, the use of older antidepressants such as monoamine oxidase inhibitors and tricyclic antidepressants is decreasing rapidly, mainly due to their adverse effect profiles. In contrast, the use of serotonin reuptake inhibitors and newer antidepressants, which have dual… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1

Citation Types

0
1
0

Year Published

2011
2011
2015
2015

Publication Types

Select...
3

Relationship

0
3

Authors

Journals

citations
Cited by 3 publications
(1 citation statement)
references
References 205 publications
(402 reference statements)
0
1
0
Order By: Relevance
“… 10 , 11 Other possible disease mechanisms that have been suggested include changes in glutamatergic neurotransmission, reduced neurotransmission of gamma-butyric acid, abnormal circadian rhythms, deficient neurosteroid synthesis, impaired endogenous opioid function, acetylcholine imbalance, tyroxine abnormalities, and dysfunction of specific brain structures and circuits. 12 In spite of these new hypotheses, one of the oldest, the monoamine hypothesis which postulates a deficiency of serotonin (5-HT) and/or norepinephrine (NE) neurotransmission in the brain, 13 , 14 is still driving clinical development of new antidepressants. Virtually all currently available antidepressants act on one or more mechanisms compatible with the monoamine hypothesis: inhibition of reuptake of 5-HT or NE; antagonism of presynaptic inhibitory 5-HT or NE receptors; or inhibition of monoamine oxidase.…”
Section: Introductionmentioning
confidence: 99%
“… 10 , 11 Other possible disease mechanisms that have been suggested include changes in glutamatergic neurotransmission, reduced neurotransmission of gamma-butyric acid, abnormal circadian rhythms, deficient neurosteroid synthesis, impaired endogenous opioid function, acetylcholine imbalance, tyroxine abnormalities, and dysfunction of specific brain structures and circuits. 12 In spite of these new hypotheses, one of the oldest, the monoamine hypothesis which postulates a deficiency of serotonin (5-HT) and/or norepinephrine (NE) neurotransmission in the brain, 13 , 14 is still driving clinical development of new antidepressants. Virtually all currently available antidepressants act on one or more mechanisms compatible with the monoamine hypothesis: inhibition of reuptake of 5-HT or NE; antagonism of presynaptic inhibitory 5-HT or NE receptors; or inhibition of monoamine oxidase.…”
Section: Introductionmentioning
confidence: 99%