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Several theories concerning the biologically based cause of depression have been suggested over the years, including theories revolving around monoamine neurotransmitters, neuroplasticity, neurogenesis, inflammation and the circadian rhythm. Physical illnesses, including hypothyroidism and mitochondrial disease, can also trigger depressive ...
Management of depression is the treatment of depression that may involve a number of different therapies: medications, behavior therapy, psychotherapy, and medical devices. Depression is a symptom of some physical diseases; a side effect of some drugs and medical treatments; and a symptom of some mood disorders such as major depressive disorder ...
Depression is commonly attributed to a deficiency in monoamines, such as serotonin. The monoamine hypothesis of depression suggests that depression is primarily caused by a deficiency of several monoamines, namely serotonin, dopamine and norepinephrine. [2] This hypothesis is widely accepted due to its simplicity. [3]
A dopamine reuptake inhibitor (DRI) is a class of drug which acts as a reuptake inhibitor of the monoamine neurotransmitter dopamine by blocking the action of the dopamine transporter (DAT). Reuptake inhibition is achieved when extracellular dopamine not absorbed by the postsynaptic neuron is blocked from re-entering the presynaptic neuron.
L-DOPA is used medically under the name levodopa in the treatment of Parkinson's disease and certain other medical conditions. It is usually used in combination with a peripherally selective aromatic L-amino acid decarboxylase (AAAD) inhibitor such as carbidopa or benserazide. These agents increase the strength and duration of levodopa.
The exact changes in brain chemistry and function that cause either late-life or earlier-onset depression are unknown. Certain theories claim that late-life depression may result from dopamine and norepinephrine misregulation. Additionally, pituitary and adrenal imbalances accompany typical cases of late-life depression.
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