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Re: Hey Linkadge!

Posted by linkadge on July 2, 2008, at 23:42:28

In reply to Re: Hey Linkadge! linkadge, posted by Marty on July 1, 2008, at 15:31:06

Well, in response to the link I would still contend that there is no in vivo demonstration that the long term use of most psychotropic drugs actually protects or reverses the neurodegenerative effects of anxiety/depression.

Sure, certain antidepressants have been shown to *influence* neurogenesis, but we are still far from concluding that this will infact restore the damage done from depression.

For instance, certain studies on the effects of SSRI's on neurogenesis has revealed that the drugs may really be simply enhancing neuronal turnover (ie they also increase neuronal elimination) rather than neurogenesis.

See:

http://www.jneurosci.org/cgi/content/abstract/25/5/1089

The following studies show that while tianeptine has a clear ability to protect the hippocampus from the effects of stress, fluoxetine has no such protective effect.

http://www.tianeptine.com/stressmorphcog.html
http://www.ncbi.nlm.nih.gov/pubmed/17561824

The following study showed that fluoxetine actually lowered long term potentiation in non stressed rats and did not pretect stress rats from the reduction in LTP. It also blocked the ability of tianeptine to restore stress induced LTP

http://www.ncbi.nlm.nih.gov/pubmed/11978839

The next study showed that tianeptine blocked stress induced neuronal atrophy but uptake inhibitors prozac or luvox did not.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T1J-3WF81YJ-G&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=b62be9fd8e9027e8caaf6a40a8b381c6

In addition, not all studies demonstrate that antidepressants actually do increase BDNF in any consistant fashion. This study found no effect of prozac on BDNF expression:

http://biopsychiatry.com/bdnfantidep.htm

This study found no effect of lithium on BDNF or BCL-2 levels:

http://www.ingentaconnect.com/content/mksg/pto/2007/00000100/00000005/art00012

Also, lithium is not always neuroprotective. In certain cases it can be highly neurotoxic. Sometimes this happens within theraputic levels, during certain affective states, or when combined with other drugs.

http://www.cogsci.ecs.soton.ac.uk/cgi/psyc/newpsy?7.32


We must be cautious on two counts. Antidepressant induced increase in neurogenesis has only been demonstrated in animals *and* it has not been consistantly demonstrated in animals.

The following study shows that prozac did not increase neurogenesis in adult mice - only in adolecent mice *and* it did not produce any neurogenesis in mice with previous exposure to early life stress!:

http://www.ncbi.nlm.nih.gov/pubmed/18512685?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

This study discusses how prozac alters behavior but *not* neurogenesis in a certain mouse strain.

http://www.ncbi.nlm.nih.gov/pubmed/18202694?ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

This study demonstrates that prozac works in this mouse strain without affecting neurogenesis:

http://www.ncbi.nlm.nih.gov/pubmed/17429410?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=1&log$=relatedarticles&logdbfrom=pubmed

I still contend that there is indeed very little proof that antidepressants actaully *correct the hippocampal atrophy seen in depression*. Like I said above, sure studies show that you can increase hippocampal turnover and perhaps cause certain cell forms to proliferate, but that doesn't necessarily equate to a larger hippocampus. Also, the acute stimulatory effects of serotonin on cell birth may not cary through after a few months. Other brain chemicals promote neurogenesis too - acetycholine, dopamine, norepinephrine etc. Hippocampal placticity may infact be impaired if the drug raises serotonin levels too high, at the cost of other brain chemicals.

The idea that all psychiatric meds induce neurogenesis is not true. Many psychiatric meds have questionable ability to induce neurogenesis and as mentioned above this does not necessarily equate to a reversal of atrophy.

This study found that lithium did not promote neurogenesis:

http://www3.interscience.wiley.com/journal/118870987/abstract?CRETRY=1&SRETRY=0

Some drugs like valrpoate are simultaniously neurotrophic and neurotoxic. (Who knows what the net long term effect will be?) Tegretol and lamotrigine are not neurotrophic but are neurotoxic. The benzodiazapines are not neurotrophic but are neurotoxic.

The word is certainly not out on antipsychotics. The typical AP's are associated with brain atrophy. The AP's are associated with faster decline of dementia and alzheimers patients despite initial hopes of cognative enhancement.

Risperidal downregulates BDNF.

http://www.ncbi.nlm.nih.gov/pubmed/12393228

Seroquel and olanzapine might have some mild benificial effect, but they both cause diabeties and metabolic disorders which is going to take a massive toll on brain health.

This study suggests that olanzapine does not have a major impact on neurogenesis, or neuronal survival.

http://cat.inist.fr/?aModele=afficheN&cpsidt=15892410

Also, dopamine signaling is neurotrophic so I would assume that long term blockade of dopamine receptors would lead to atrophy.

That leaves you with the antidepressants. As mentioned above not all studies demonstrate neurogenesis with the antidepressants, not all studies support the idea that antidepressants do infact lead to a net increase in number of surviving brain cells. In addition, many studies show that tianeptine but not the SSRI's has a preventative effect on stress induced hippocampal atrophy. Many studies find that antidepressants and lithium do not affect BDNF signalling in a consistant or prolonged way. Finally, virtually no studies (in humans) have infact demonstrated that antidepressant treatment leads any significant amelioration of brain atrophy associated with depression.

I.e. the link you gave refereneces a framework of potential benefits, based on certain mouse studies and some theorization.

The only reason I put tianeptine above the other treatments is that in any study I have seen that compares tianeptine to other AD's for their neuroprotective capacity, tianeptine always comes out far ahead. Its true that tianeptine's neuroprotective effects have not been done in humans but I believe the rodent studies are at least a little more consistent.


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URL: http://www.dr-bob.org/babble/20080626/msgs/837783.html