Talk:Reelin

message: The second role of reelin controls neuroplasticity and uses the same molecular mechanisms as the neurodevelopmental functions.
1. Reelin is excreted into the extracellular space of the brain by Cajal Retzius cells near the brain surface. It seeps down to the middle pyramidal layer of the grey matter where pyramidal and intermediate neurones expresses reelin receptors.  These receptors are similar to VLDL or cholesterol receptors. (This significance of this is uncertain but is interesting because of the relationship between ApoE3 and Alzheimers disease). 
The stimulation of reelin then triggers a phosphokinase mechanism which encourages the production of mRNA and the production of actin.  Actin is a "muscle protein" which then allows the neurone to actively alter its shape
via "dendritic spines". The dendritic spines carry synapses which allow neurones to communicate with each other. (The synapses in the prefrontal cortex carry GLU or NDMA receptors).  The phosphokinase receptor complex is a very large and complex molecule composed of several subunits.  One subunit is the Fragile X protein.  This is an abnormal protein that is associated with the commonest (known) from of inherited mental retardation and the Fragile X syndrome is also associated with an increased incidence of schizophrenia.
... end of removed text. Andrewa 19:44, 17 May 2004 (UTC)
thread_title: Neuroplasticity

message: here is a great graphical illustration of the difference in corticogenesis between the "normal" and the "reeler" mice. Alas, as I understand, the image is copyrighted. But it is quite simple drawing. If somebody will re-draw the image and upload free version on the Reelin page, it would be great!--CopperKettle 16:35, 30 May 2006 (UTC)
thread_title: '''Plea for help to people skilled with graphics'''

message: # Write in more detail about the DNMT1-induced hypermethylation of RELN promoter region (CpG islands)
# Read on amphetamine-induced decrease in RELN expression. 
--CopperKettle 17:38, 12 February 2007 (UTC)
thread_title:  To Do list 

message: # Reelin pathway and.. pancreatic cancer --CopperKettle 05:53, 14 February 2007 (UTC)
thread_title:  To Read 

message: A note to myself:
* A polymorphic GGC triplet repeat located in the 5'-UTR region of RELN gene, which harbors in the normal population 8 to 10 repeats, is significantly increased in autistic patients to carry 4 to 23 additional repeat - find the source, maybe add to the "autism" section. --CopperKettle (talk) 13:08, 10 December 2008 (UTC)
thread_title:  Autism 

message: These edits add some facts but also there is an additional claim that reelin-schizophrenia link is very weak; that may be, and I am all for the good "critique" paragraph, with sources or explanations why reelin may be a false lead. Best regards, --CopperKettle (talk) 15:29, 25 December 2008 (UTC)
replies: text: I havent really understood this bit: this result implied that they were receptors it was the later papers that demonstrated Reelin binding that confirmed this identity. - did the paper was the first to acknowledge that VLDLR and ApoER2 are receptors? From the abstract, it seems that they are mentioned as receptors, as if it was already known. --CopperKettle (talk) 15:34, 25 December 2008 (UTC)
replies: text: But as for the "Most scientists don't accept these inflated claims.", " this is not generally accepted." - these are very bold statements; there should be references at least to the blog or media publicatons. --CopperKettle (talk) 15:45, 25 December 2008 (UTC)
thread_title:  Interesting anonymous edits (25 dec 08) 

message: I quote: "In 1994 a new allele of reeler was obtained by insertional mutagenesis (Miao et al., 1994)". Is this the right phrasing? I do not fully understand that this means, maybe it should be rephrased or the terms wiki-linked to appropriate articles for further "self-study". --CopperKettle (talk) 02:44, 26 December 2008 (UTC)
thread_title:  A new allele was obtained 

message: * A quote from the article: One study indicated the upregulation of histone deacetylase HDAC1 in the hippocampi of patients.[109] - but HDAC1 may be protective against injury:"Indeed, reducing HDAC1 activity using small interfering RNA or a specific inhibitor in cultured cortical neurons or in vivo resulted in increased numbers of DNA double strand breaks (DSBs), the expression of cell cycle proteins and cell death. Increasing HDAC1 function by overexpressing it had the opposite effect, protecting cells against DSBs and neurotoxicity." Hmm.. what if HDAC1 increase is the brains' reply to toxic medication.. --CopperKettle 04:58, 16 February 2009 (UTC)
thread_title:  Interesting bit 

message: The addition by User:DavidJWu seems to be too extensive and a bit loosely related (IMHO):Kanner in 1943 was the first to report on the neurological disorder autism and among his many observations he noticed that a portion of his cohort had enlarged heads.Kanner, L., Autistic disturbances of affective contact. Nervous Child 1943. 2: p. 217-250. This observation of macrocephaly was corroborated by numerous studies and some suggest that accelerated growth is an early warning sign of risk of autism.Bailey, A., et al., Autism and megalencephaly. Lancet, 1993. 341(8854): p. 1225-6.Courchesne, E., R. Carper, and N. Akshoomoff, Evidence of brain overgrowth in the first year of life in autism. Jama, 2003. 290(3): p. 337-44.Palmen, S.J., et al., Neuropathological findings in autism. Brain, 2004. 127(Pt 12): p. 2572-83.Fidler, D.J., J.N. Bailey, and S.L. Smalley, Macrocephaly in autism and other pervasive developmental disorders. Dev Med Child Neurol, 2000. 42(11): p. 737-40. These studies led researchers to examine the neurophysiology of autistic subjects. However, the small research sample sizes lead to a lack of statistical power compounded with the natural heterogeneity of the disorder introduced many confounding variables that have made results inconclusive. What has been concluded thus far is that there is a decrease number of Purkinje cells throughout the cerebellum and cortical dysgenesis reminiscent of the reeler mouse.Palmen, S.J., et al., Neuropathological findings in autism. Brain, 2004. 127(Pt 12): p. 2572-83.
 	In 2002, Fatemi et al. measured the blood levels of unprocessed Reelin in 28 autistic twins, their parents and siblings. A statistically significant reduction of the unprocessed Reelin was found in the twins along with their parents and even unaffected siblings when compared to controls.Fatemi, S.H., J.M. Stary, and E.A. Egan, Reduced blood levels of reelin as a vulnerability factor in pathophysiology of autistic disorder. Cell Mol Neurobiol, 2002. 22(2): p. 139-52. Despite the inconclusive neuropathology studies, some abnormalities were reminiscent of the reeler neuropathology and the identification of reduced Reelin levels by Fatemi et al. led to the genomic screening of reelin.
 		Autistic family and twin studies have suggested that genetic factors might lead to a predisposition of autism.Steffenburg, S., et al., A twin study of autism in Denmark, Finland, Iceland, Norway and Sweden. J Child Psychol Psychiatry, 1989. 30(3): p. 405-16. The proposition by many is that reelin is one of those candidate genes for autism. Studying 95 autistic subjects, Itailian in ethnicity, and 186 matched controls, there was a significant association with a polymorphic repeat located immediately preceding the 5’ ATG initiator codon of reelin.Persico, A., et al., Reelin gene alleles and haplotypes as a factor predisposing to autistic disorder. Molecular Psychiatry, 2001. 6: p. 150-159. Longer triplet repeats in the 5’ region were associated with an increase in autism susceptibility. The 5’ end of reelin was further analyzed using 125 multiple-incidence families. There was no significant difference between the length of repeats found between affected and controls however, family based association test found that larger reelin alleles were transmitted more frequently than expected to affected childrenZhang, H., et al., Reelin gene alleles and susceptibility to autism spectrum disorders. Mol Psychiatry, 2002. 7(9): p. 1012-7..
* Why is there a whole paragraph on large heads? 
* Fatemi et al., 2002 is already cited by me above
* After that comes the second mention of "abnormalities reminiscent". Could be merged into one, IMHO
* General mention of genetic factor of autims could be dropped, and a "main article" template leading to the Heritability of autism article could be added to the subsection instead. 
Best regards, --CopperKettle 13:54, 1 June 2009 (UTC)
replies: text: That whole section was way too long as a summary of Reelin and autism. Also, it cited primary studies, where it should be citing reliable reviews (as per WP:MEDRS). I took a crack at the problem by rewriting the section to make it briefer and to cite a reliable review, Pardo et al. 2007 (). Eubulides (talk) 20:52, 1 June 2009 (UTC)
thread_title: Addition to the "Autism" section

message: I've completed my test attempt to convert a portion of the article to the WP:LDR reference style.
The test included the lead, and first three sections (through Tissue distribution and secretion)
Results can be seen here
The view will look slightly different, because the TOC is shorter.
(edit - see also reelin testing take 2 for sample with only the LDR change)
I made two types of changes, the first of which is the main point and more significant:
# I converted the references to LDR style, the goal of which is to move the bulk of the reference to the reference section and leave only a stub in the main article
# When there were two citations for the same point, I combined the two citations into a single footnote
Covering the second item first, I think that while the presence of footnotes helps signal that it is a professional article, the existence of footnotes detracts from the appearance, so if I can use one footnote instead of two, I think it looks better. Note importantly that this decision is independent of the LDR decision; combining of citations into a single footnote can be done or not, in either LDR or traditional citation style. If you object to this combination, I can do the LDR without it. Implementing it will slightly change the footnote numbering, as old footnote 1 and 2 are now footnote 1.
The bigger change is the use of LDR.
The first four sections took up 20.7K of space. When I convert to LDR, the aggregate space used is up slightly, but the main article space now takes up 10.2K, and the Reference section takes up 12.4K. In other words, this article have more bytes devoted to references than to text. This isn't meant to imply anything good or bad regarding content, what it means is that an editor trying to find one's way through the edit text has to wend one's way through more reference material than non-reference material. Whomever organized it did a clever job of separating out the footnotes, but it is still a chore to read the material in edit mode, when you are trying to find exactly where to make an edit change. 
The revised version is much easier to edit. The visual impact of the article to the reader is virtually unchanged (the only change is due to combining citations), but the LDR conversion changed nothing about the reader impression. 
However, the visual view to the editor is much improved, as it looks more like the original article. It still has  interspersed in the article, but that's far less visually distracting than the full citation.
As a minor note, I now have each reference in the reference section separated by a blank line, so it is relatively easy to scan through all the references.
It's a fair amount of work to do the complete conversion, so I would like to get a consensus of those who regularly edit this page before proceeding. I hope you will agree it is worth doing, but I'd hate to invest the time necessary, and then have someone simply revert it.--SPhilbrickT 21:13, 8 October 2009 (UTC)
replies: text: I rather like it.  Two thumbs up from me.  (Though I do think that each reference should have its own footnote.  More closely mirrors how most journals do it...)  Nice job...  Cheers, AndrewGNF (talk) 21:54, 8 October 2009 (UTC)
replies: text:  I'm all for the change, thank you, Sphilbrick! But I'm also unsure of combining article references into single footnotes. I usually combine into a single footnote a ref to a journal article only with some popular reviews on the same matter (in press\blogs). --CopperKettle 03:29, 9 October 2009 (UTC)
replies: text:  I am all for the change to LDR style since it makes the raw wiki text much less clutter and easier to read and edit.  I am not so sure about combining references however.  The same reference is sometimes used more than once in the same article.  In one section citing a group of references might be appropriate but in another section, only one reference of from this same group might be appropriate to cite.  Combining references would also interfere with the use of the  template (see for example Benzodiazepine#Side_effects, where references 22 with a specific page number and 59 are cited together). Finally I note that a  script to convert references in an article to LDR style.  This works great if the same reference is not cited more than once but messes up when the same reference is cited more than once.  Hopefully this bug will be worked out since it would make these conversions much easier to carry out.  Cheers.  Boghog (talk) 05:24, 9 October 2009 (UTC)
replies: text: Ironically, one of the first things I worked on with LDR was a situation where someone had seven or eight references for the same claim, and didn't like the look, so we combined them to improve the visual appearance. That said, I understand that it isn't typical scientific style. I'll redo the example to see it with one citation per footnote. Thanks, Boghog, for pointing out the script. I had asked at Village Pump, but hadn't recevied an aswer. I'll check it out.--SPhilbrickT 11:20, 9 October 2009 (UTC)
replies: text: So far, there's positive response for the modified change. I'm leaving for Zurich for a week, and don't to start something, then have a problem and leave anything in error, so I'll wait till I return next week.--SPhilbrickT 02:55, 11 October 2009 (UTC)
thread_title:  Test attempt see if the article could be improved using LDR citation style 

message: I interpret the discussion above to be a consensus for trying the change, but not doing the combination of citations.
I plan to start doing the conversion about 1PM EDT. I mention this because it will be helpful if others do not make edits while I am doing the changes. While I will endeavor to make each edit stand on its own, without going into gory details, intervening edits makes my job a bit harder. 
I will post a notice on the page, and remove it when I'm done or take a break. 
If anyone wants to make a change, and doesn't want to wait, post a note to my talk page and I'll take a break. --SPhilbrickT 15:36, 23 October 2009 (UTC)
thread_title:  LDR citation conversion 

message: I see "Reelin" is written almost everywhere in this article with a capital, but is this necessary? The Wiki ghost (talk) 08:32, 30 April 2010 (UTC)
thread_title: Capital

message: In the explanation of the cause of this disorder it states that the cDNA of the reelin gene is improperly spliced - this doesn't make sense as there is no cDNA in a cell (cDNA is complementary DNA, created from a mature mRNA transcript and is not the same as mRNA).  It looks to me that whoever wrote this part just quoted straight off of the reference without really thinking about it - I have changed cDNA to mRNA transcript.
Prudhommei1 (talk) 02:15, 21 February 2011 (UTC)
thread_title: Issue with Lissencephaly Section

message: The mouse homologue, Reln, is located on mouse chromosome 5. 7q22 is the location of the human homologue, RELN. The article should be edited to reflect this (currently no time to do this myself). --Crusio (talk) 06:32, 24 November 2011 (UTC)
thread_title:  Location 

message: I'm busy elsewhere; will look into the issue in late July:  Heterozygous Reelin Mutations Cause Autosomal-Dominant Lateral Temporal Epilepsy --CopperKettle 06:01, 6 June 2015 (UTC)
thread_title:  One study associates RELN mutations with a form of epilepsy 

message: Loss of Reelin protects against atherosclerosis by reducing leukocyte–endothelial cell adhesion and lesion macrophage accumulation in a mice model - Rod57 (talk) 20:12, 15 March 2016 (UTC)
thread_title:  Possibly involved in atherosclerosis 

message: Hello fellow Wikipedians,
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*Added archive https://web.archive.org/web/20080917064917/http://www.schizophreniaforum.org/for/curr/grayson/default.asp to http://www.schizophreniaforum.org/for/curr/grayson/default.asp
*Added archive https://web.archive.org/web/20061125230210/http://www.inb.u-bordeaux2.fr/siteneuro2/pages/UniteINB/Manzoni/Manzoniavenir.htm to http://www.inb.u-bordeaux2.fr/siteneuro2/pages/UniteINB/Manzoni/Manzoniavenir.htm
*Added  tag to http://genetics.plosjournals.org/perlserv/?request=get-document&doi=10.1371%2Fjournal.pgen.0040028
*Added archive https://web.archive.org/web/20100913030040/http://www.schizophreniaforum.org/res/sczgene/geneoverview.asp?geneid=135 to http://www.schizophreniaforum.org/res/sczgene/geneoverview.asp?geneid=135
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thread_title:  External links modified