I have little faith
"She rules until the end of time
She gives and she takes
She rules until the end of time
She goes her own way..."
ketamine? interesting xP ...I mean yeah sounds interesting!
I don't believe depression works like that
I've heard about using drugs like this for depression (they've been talking about this for years). And yes I think it's promising and needs to be explored.
It's definitely a promising future treatment. The idea has been around for quite awhile now and I believe they have human clinic Ketamine studies running at the moment. It's been called 'ECT in pill form'. It's one of the growing future treatments for treatment resistant depression along with Transcranial magnetic stimulation.
More on Ketamine trials:
And Transcranial Magnetic Stimulation:
http://www.nih.gov/news/health/jun2011/nimh-22.htmDrug boosts growth factor to jump-start rapid antidepressant response
Little-known enzyme pivotal — NIH-funded study in mice
A study in mice has pinpointed a pivotal new player in triggering the rapid antidepressant response produced by ketamine. By deactivating a little-known enzyme, the drug takes the brakes off rapid synthesis of a key growth factor thought to lift depression, say researchers supported by the National Institutes of Health.
Earlier studies had shown that the growth factor, called brain-derived neurotrophic factor (BDNF), produces antidepressant-like effects. To find out if BDNF is involved in ketamine’s action, the researchers gave the drug to mice genetically engineered to lack BDNF. Unlike in control mice, ketamine failed to produce a fast-acting antidepressant-like response in such BDNF knockout mice exposed to experimental situations that trigger depression-like behaviors. This and other tests confirmed that ketamine’s rapid antidepressant effects depend on rapid synthesis of BDNF in the brain’s memory center, or hippocampus.
The researchers determined that this happens so quickly — within 30 minutes — because time-consuming intermediate steps have already been completed. It only requires the translation of BDNF mRNA, an intermediate form, into the final protein. By contrast, conventional antidepressants are thought to work through a much more lengthy and indirect process that requires, among other things, the birth of new neurons and their integration into circuits.
Ketamine achieves this boost in BDNF levels by first blocking a protein on neurons (brain cells) called the NMDA receptor. The Texas team discovered that this blockade, in turn, deactivates an enzyme called eukaryotic elongation factor 2 (eEF2) kinase, which restrains BDNF synthesis. So ketamine (and presumably other agents that similarly turn off the enzyme) effectively takes the brakes off of this antidepressant mechanism.
More interesting finding's: Memantine (which works in a similar albeit milder fashion to Ketamine) has been shown in a recent trial to rapidly help alleviate depressive symptoms.
http://bipolarnews.org/?p=1110Memantine (Namenda), which is approved by the Federal Drug Administration (FDA) for use in Alzheimer’s Dementia, is increasingly being used for other conditions. Some doctors prescribe memantine for hyperactivity and attention problems in attention deficit hyperactivity disorder (ADHD), for obsessive compulsive disorder (OCD), and most recently as an adjunct to lamotrigine in bipolar depression. We wrote about the findings of Amit Anand et al. on the use of memantine and lamotrigine in January. These findings have just been published in Bipolar Disorders. The study indicates that the combination of lamotrigine with memantine brought about a rapid onset and greater magnitude of antidepressant effects than the combination of lamotrigine and placebo.
^ That said, it would be the first 'decent' generation of 'real' antidepressants. . .
I wouldn't take anything that present medicine has to offer, not that I haven't tried it.
If depression is caused (or can be caused) by a a chemical imbalance in the brain, then why wouldn't that work?
Looks like another step forward in this direction is in the works!
http://www.scienceagogo.com/news/201...runc_sys.shtmlSuccessful clinical trial for ketamine-like antidepressant
Researchers are reporting a successful phase IIa clinical trial of GLYX-13, a first-of-its-kind ketamine-like antidepressant that takes effect within 24 hours and delivers double the antidepressant effect of traditional selective serotonin re-uptake inhibitor (SSRI) treatments. Details of the clinical development of GLYX-13 appear in the current issue of the journal Neuropsychopharmacology and the trial results were presented last Thursday at the 51st Annual Meeting of the American College of Neuropsychopharmacology.
GLYX-13 works by modulating the N-methyl-D-aspartate (NMDA) receptor in the brain, as do other NMDA receptor antagonists such as ketamine, but GLYX-13 does not have their serious and limiting side effects, such as hallucinations and schizophrenia-like effects. NMDA receptors play a key role in regulating synaptic plasticity - the quality of the connection between neurons - and thus are important in regulating learning and memory functions.
In trials administered at 12 sites across the country, a single dose of GLYX-13 resulted in significant reductions in depression symptoms among subjects who had shown little improvement with previous drugs. The positive effects of GLYX-13 were evident within 24 hours and lasted an average of seven days. The effect size, a measure of the magnitude of the drug's antidepressant efficacy, at both these times after a single dose was nearly double the effect size seen with most other antidepressant drugs after four to six weeks of repeated dosing. Side effects of GLYX-13 were mild to moderate and were consistent with those observed in subjects receiving a placebo.
Uncovering the Biology of Depression
Professor of Psychiatry and Pharmacology Director at Yale University, Ronald Duman studies depression, a serious issue that affects approximately 17% of the U.S. population and is estimated to cost as much as $83.1 billion for our economy. There is a general consensus in the scientific community that low levels of monoamine neurotransmitters are a major contributor of depression. From that belief, antidepressants are designed to increase levels of neurotransmitters in the brain. A diverse range of antidepressants exists. However, current antidepressants are still ineffective and have low response rates: only 1 in 3 respond to the first antidepressant treatment, and 2 in 3 ever respond after repeated treatments. Beyond knowing that antidepressants block or inhibit particular neurotransmitters, most scientists are still not sure which pathways these antidepressants influence and thus the types of mechanisms that contribute to depression. Duman’s work investigates these unknown pathways.
Neurotrophic Theory of Depression
The bulk of Professor Duman’s research has led to the formulation of the neurotrophic theory of depression, which states that neuronal growth factors contribute to the onset of depression. In 1995, Duman published a landmark paper relating increased brain derived neurotrophic factor (BDNF) levels with antidepressant effects, setting the foundation for the neurotrophic hypothesis of depression.
The Role of BDNF
BDNF is a vital neurotrophic factor in the brain. Previous studies have shown that exposure to BDNF in the hippocampus can lead to increased strength in some synaptic connections. BDNF’s role in neurogenesis was of particular interest. Duman discovered that upregulation of neurogenesis was the result of several antidepressants, suggesting that antidepressants reverse the atrophy of neurons that occur during depression. Other studies confirming Dr. Duman’s work have found that increasing levels of BDNF in specific areas of the brain, such as the hippocampus, leads to antidepressant effects. The hippocampus has been implicated in mood disorders and its connections to amygdala and the prefrontal cortex are important for the function of cognition and emotion. Additionally, studies by Duman also revealed the converse: loss of BDNF contributes to depression. Stress, a precursor of many mood disorders, also decreases expression of BDNF.
A Faster and More Efficient Pathway
In August 2010, Duman’s lab discovered a completely new pathway, a major breakthrough for the field of depression. In ketamine, Duman addresses a pressing need in the field for “a more rapid, more efficient drug” to treat depression. In his paper published in Science, Duman lays the foundation for further understanding of this novel pathway.
Ten years ago, ketamine was preliminarily tested at the Connecticut Mental Health Center as an antidepressant in low doses. The subjects were patients who previously resisted all other forms of treatment, but over two thirds responded positively to ketamine. These results were confirmed in later studies. Much more remarkable about ketamine’s use as an antidepressant was how quickly the patients responded; antidepressant effects took place within two hours of treatment and lasted more than seven days.
Studies conducted by graduate student Nick Li demonstrate that ketamine activates the mammalian target of rapamycin (mTor) pathway. mTor is a ubiquitous protein kinase involved in protein synthesis and synaptic plasticity in a process called synaptogenesis. Synaptogenesis restores the synapse connections in the brain that may deteriorate under stress and depression.
Ketamine is such a “magic drug” because it produces antidepressant effects in people who have resisted most other forms of treatment and its speed of response acts in days rather than weeks. However, the key disadvantages of directly using ketamine as an antidepressant are its use as a street drug and its toxicity from repeated dosages. Despite these shortcomings, knowing the mechanisms of ketamine’s antidepressant effects will further benefit drug designs for immediate antidepressant effects.