5 replies to this topic

[Ghostrider]

How do you know that your memory has gone to hell due to accutane alone? Are there are other possible factors affecting your preception?

[Ghostrider]

Wiserules, it has been scientifically proven that smoking copious amounts of marijuana will have a deleterious effect on your memory. Regardless of whether you continue or discontinue accutane, if you really care about cognitive function, the marijuana must go immediately. I don't understand why some people come to this forum looking for cognitive enhancement while they continue to use recreational drugs. How how can you compare someone's current memory state to what it was last week or a month ago? Would you be able to detect even a 20% change in cognitive function?

[Ghostrider]

Humm...are you currently taking accutane? If not, then how long ago did you take it? I took accutane several years ago, since I did not challenge myself in high school, I don't remember if it affected my memory at all (no pun intended :-). However, I can say with certainty that my memory improved by several magnitudes in college where I challenged myself to learn. Part of the memory problem could be linked to being uninterested in learning or perhaps depression -- which Accutane has been linked to.

[dank]

Sakai Y, Crandall JE, Brodsky J, McCaffery P. 13-cis Retinoic acid (accutane) suppresses hippocampal cell survival in mice. Ann N Y Acad Sci. 2004 Jun;1021:436-40.

UMMS/E.K. Shriver Center, 200 Trapelo Rd., Waltham, MA 02452, USA.

Use of the acne drug Accutane (13-cis retinoic acid, [13-cis RA]) has been associated with severe depression. This association has been considered controversial because no causative link has been found between 13-cis RA and this disorder. A recent hypothesis has suggested that atrophy of the hippocampus can result in depression. We now show, in a mouse model, that endogenous RA generated by synthetic enzymes in the meninges acts on hippocampal granule neurons, and chronic (3-week) exposure to a clinical dose of 13-cis RA may result in hippocampal cell loss. In humans this may be conjectured to be the mechanism by which Accutane contributes to depression.

PMID: 15251924 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm....l=pubmed_docsum

##

Lane MA, Bailey SJ. Role of retinoid signalling in the adult brain. Prog Neurobiol. 2005 Mar;75(4):275-93.

Department of Human Ecology, Division of Nutritional Sciences, The University of Texas at Austin, Austin, TX 78712, USA. mlane@mail.utexas.edu

Vitamin A (all-trans-retinol) is the parent compound of a family of natural and synthetic compounds, the retinoids. Retinoids regulate gene transcription in numerous cells and tissues by binding to nuclear retinoid receptor proteins, which act as transcription factors. Much of the research conducted on retinoid signalling in the nervous system has focussed on developmental effects in the embryonic or early postnatal brain. Here, we review the increasing body of evidence indicating that retinoid signalling plays an important role in the function of the mature brain. Components of the metabolic pathway for retinoids have been identified in adult brain tissues, suggesting that all-trans-retinoic acid (ATRA) can be synthesized in discrete regions of the brain. The distribution of retinoid receptor proteins in the adult nervous system is different from that seen during development; and suggests that retinoid signalling is likely to have a physiological role in adult cortex, amygdala, hypothalamus, hippocampus, striatum and associated brain regions. A number of neuronal specific genes contain recognition sequences for the retinoid receptor proteins and can be directly regulated by retinoids. Disruption of retinoid signalling pathways in rodent models indicates their involvement in regulating synaptic plasticity and associated learning and memory behaviours. Retinoid signalling pathways have also been implicated in the pathophysiology of Alzheimer's disease, schizophrenia and depression. Overall, the data underscore the likely importance of adequate nutritional Vitamin A status for adult brain function and highlight retinoid signalling pathways as potential novel therapeutic targets for neurological diseases.

PMID: 15882777 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm....l=pubmed_docsum

##

Chambon, et. al. Regulation of dopaminergic pathways by retinoids: activation of the D2 receptor promoter by members of the retinoic acid receptor-retinoid X receptor family. Proc Natl Acad Sci U S A. 1997 Dec 23;94(26):14349-54.

Dopamine is a neuromodulator involved in the control of key physiological functions. Dopamine-dependent signal transduction is activated through the interaction with membrane receptors of the seven-transmembrane domain G protein-coupled family. Among them, dopamine D2 receptor is highly expressed in the striatum and the pituitary gland as well as by mesencephalic dopaminergic neurons. Lack of D2 receptors in mice leads to a locomotor parkinsonian-like phenotype and to pituitary tumors. The D2 receptor promoter has characteristics of a housekeeping gene. However, the restricted expression of this gene to particular neurons and cells points to a strict regulation of its expression by cell-specific transcription factors. We demonstrate here that the D2 receptor promoter contains a functional retinoic acid response element. Furthermore, analysis of retinoic acid receptor-null mice supports our finding and shows that in these animals D2 receptor expression is reduced. This finding assigns to retinoids an important role in the control of gene expression in the central nervous system.

[PMID: 9405615]

http://www.ncbi.nlm....l=pubmed_docsum

##

Boudjelal M, Voorhees JJ, Fisher GJ. Retinoid signaling is attenuated by proteasome-mediated degradation of retinoid receptors in human keratinocyte HaCaT cells. Exp Cell Res. 2002 Mar 10;274(1):130-7.

Department of Dermatology, University of Michigan, Ann Arbor, Michigan 48109, USA.

The biological actions of retinoids are mediated by nuclear retinoid receptors, RAR and RXR, which are ligand-activated transcription factors. We investigated the mechanism of attenuation of retinoid receptor activity in human keratinocyte HaCaT cells. Treatment of HaCaT cells with all-trans-retinoic acid or 9-cis-retinoic acid reduced RARgamma and RXRalpha protein levels by one-half within 24 h. In contrast, retinoid treatment did not alter RARgamma or RXRalpha mRNA levels, suggesting that retinoids stimulate breakdown of their receptors. Pulse-chase studies revealed that retinoid treatment of HaCaT cells reduced RARgamma and RXRalpha half-lives by 50%, indicating that retinoids accelerate breakdown of their receptors. The proteasome inhibitor MG132 prevented retinoid-induced receptor loss. Furthermore, MG132 potentiated retinoid-induced receptor activity, as assessed by expression of the retinoid-regulated CRABP-II gene in HaCaT cells. These data demonstrate that retinoids attenuate retinoid receptor function by enhancing proteasome-mediated retinoid receptor breakdown in HaCaT cells. Proteasome-mediated degradation of RARgamma or RXRalpha in vitro was significantly reduced by the corepressor SMRT, which binds unliganded retinoid receptors. This protection from degradation was markedly diminished by ligand, which causes SMRT to dissociate from receptors. Ligand failed to relieve protection from degradation by SMRT of a mutant form of RXRalpha that binds SMRT in the presence and absence of ligand. Addition of coactivators TIF1, TIF2, and RIP140 had no effect on degradation of RARgamma or RXRalpha. In summary, ligand binding to retinoid receptors promotes proteasome-mediated receptor degradation via dissociation of SMRT. Ligand-stimulated receptor degradation results in attenuation of retinoid signaling. Copyright 2002 Elsevier Science (USA).

PMID: 11855864 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm....l=pubmed_docsum

I have plenty more abstracts demonstrating that her memory loss is more than a plausible result of her Accutane treatment. Contact me: accutaneinfo[at]yahoo.com

Edited by dank, 15 September 2006 - 09:55 AM.

[roberts_cole]

Hi, I will preface my comment by the admission that I have not yet read the latest literature on accutane and its effects on cognitive functioning. However, it quite likely that you may be sufferring from some degree of depression. Accutane is known to cause to depression and that alone could account for any cognivitve changes that you may have experienced. I myself used accutane in my late teens (read just over a decade ago). I recall eperiencing many side-effects such as extremely dry skin as well as joint pain and pruritis. The dry skin/mucous membranes such as eyes, has been an ongoing side effect even years after my discontinuation of accutane. In retrospect, my gpa declined slightly during the period of time that I was using accutane.

There was a few people in my medical school that had to take time off, and effectively lost a year of education, from accutane-induced depressive episodes. In short, on the positive side, accutane worked amazingly well at getting rid of my acne to the point that I too this day, never ever get pimples, yet I experience on-going trouble with dry skin, eyes, and god-only knows what other residual effects.