Easily the most complex structure in the known universe, scientists have learned more concerning the human brain in the past 2 decades than in every one of human history combined. For doctors that study and treat mental and emotional illnesses, new knowledge has forced them to rethink some of the most firmly held beliefs. This is particularly true with regard to depression, which can be one of the most common mental problems the world over.
Tianeptine powder
Even though the factors responsible for depression are not well understood, those in the psychiatric community were fairly sure that the recurrent mental disorder was caused by abnormally low degrees of neurotransmitter substances in the brain. Therefore, the main focus of pharmacotherapy for treating depression in recent decades has gone to prescribe medications which are known to enhance levels of serotonin and other brain chemicals. It's no surprise prescription drugs in the serotonin reuptake inhibitor (SSRI) class, this kind of paroxetine, sertraline, and fluoxetine, are some of the very commonly prescribed pills on the planet. The sole problem is they may not be terribly effective in the treating major depressive disorder (MDD).
Lately, researchers have focused more attention on a fresh theory that explains the development and persistence of depression. While they do agree totally that changes in neurochemical levels are largely accountable for emotional and cognitive disruptions, investigators add that neuroplasticity - which involves structural and functional changes in how the mind processes information - may explain depressive episodes that last longer than two weeks. And because these changes are caused by persistently low quantities of neurotransmitter substances, they might be difficult to reverse with traditional pharmacological treatments such as for example SSRIs. This may explain why patients with severe depression, or MDD, tend to be more likely to need electroconvulsive shock therapy (ECT) than individuals with more mild kinds of the disorder.
With assistance from technology, researchers have found significant differences between depressed and non-depressed brains. MRIs and PET scans have revealed both structural and functional alterations in three regions of the brain that are involved in cognitive and emotional processing: the amygdala, the prefrontal cortex, and the hippocampus. Because neuroplasticity is a fact rather than theory, it makes sense that those who suffer with severe depression are more likely to have brains that look different on scans. Unlike SSRIs and other mainstream treatments for depression, an alternative solution and well-tested treatment for clinical depression addresses the likely root of the problem.
Developed in France in the 1960s, tianeptine is just a tricyclic antidepressant that has unique pharmacological properties. Unlike most antidepressants that treat the disorder by increasing serotonin levels, tianeptine's primary mechanism of action is always to modulate glutamate, that is the principal excitatory neurotransmitter in the brain.This action is believed to truly have a salubrious effect on mental performance by protecting its structural plasticity in the aforementioned regions.
In addition to significantly increasing a person's risk of developing depression, animal testing indicates that chronic stress reduces how big is dendrites (short, branched extensions) on neurons in both hippocampus and the prefrontal cortex.With smaller, weaker neurons in these regions of mental performance, it will come as not surprising that chronic stress has been strongly linked to serious impairment of the cognitive and emotional processes these areas control. These unhealthy alterations might be prevented with daily administration of tianeptine. Numerous studies have found that the tricyclic antidepressant blocks the stress-induced reduced total of dendrites in the hippocampus. Further testing in addition has revealed that since it acts as a neuronal protectant, tianeptine prevents the negative effects of chronic stress on hippocampus-based learning and memory. Neither fluoxetine (Prozac) nor fluvoxamine (Luvox) can make that claim, which is further proof of divergent cellular and molecular mechanisms between tianeptine and conventional SSRIs. Researchers have yet to determine if tianeptine protects the prefrontal cortex from stress, but that seems a likely outcome. We also know that the drug shields dendritic arbors in the amygdala from the effects of chronic stress.
The hippocampus is certainly one of only two regions in the human brain that creates new nerve cells or neurons. Referred to as neurogenesis, some researchers genuinely believe that impairment of this technique in the mind may be partly accountable for depression, especially clinical depression. Why? Because animal testing has revealed that chronic stress substantially reduces hippocampal neurogenesis and increases cell death (apoptosis) in both that region and in the temporal cortex. Long-term administration of tianeptine can prevent these unhealthy impairments by blocking stress before it does its damage. There's even some evidence that the drug may increase quantities of brain-derived neurotrophic factor (BDNF), that will be required for neurogenesis.
In the event you were wondering why you've never heard of tianeptine before or why it isn't nearly as popular as fluoxetine (Prozac), paroxetine (Paxil), or sertraline (Zoloft), it's since the drug was mislabeled being an SSRI from the start. It was not until fairly recently when it discovered that tianeptine's actions as an antidepressant were unrelated to its effect on serotonin levels. And so after significantly more than four decades on the shelf, the nearly unknown antidepressant experienced a rebirth. It is only within the last few couple of years that the majority of the great things about the drug we have discussed today were discovered. We also understand that its therapeutic effects are mostly likely because of its regulation of glutamate levels, which testing has revealed tend to be elevated in depressed patients.
