Talk:Alzheimer's disease/Archive 4
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Images
I am not sure that the histopathology picture is convincing. Where is the neurofibrilary tangle? It might be useful to show a brain scan or a photograph of a brain with increased sulci and reduced gyri (and perhaps a normal one for comparison). Snowman 23:29, 6 November 2006 (UTC)
- I've requested assistance here from a polyglot user who may be able/willing to transwiki the images on the ro: article to Commons. We'll see how it works out.LeadSongDog (talk) 21:29, 29 January 2008 (UTC)
- Also asked ro:Discuţie Utilizator:Moby Dick to help out. LeadSongDog (talk) 05:01, 31 January 2008 (UTC)
This is the Romanian AD Featured Article - it has a few pics that could be used here. Interestingly, the 'Treatment' section looks like the one here used to look like - I wonder how much, if any, of the article is a direct translation. --Matt Lewis (talk) 01:05, 17 February 2008 (UTC)
- If someone gives the English text for the image on the left in here - I'll adapt the graphic. It must be German - as it (APP-Schema.jpg) is in the German article too.--Matt Lewis (talk) 23:09, 4 March 2008 (UTC)
- Apparently it is German. See where it came fromLeadSongDog (talk) 18:33, 16 March 2008 (UTC)
Fatality
In some parts of the article (for ex. statistics) AD is stated as a cause of death. But on the other hand, no where in the article it's not stated whether AD is fatal or not. It seems like it's fatal, but not clear why, the chances, and reason. It would be nice if there's some kind of info about fatality in the first section. iyigun 23:06, 16 January 2007 (UTC)
- Many things are causes of death without being necessarily or immediately fatal to all people, immediately. Any kind of paralysis or coma, for example. These things cause such gigantic care problems for any person that the patient becomes practically impossible to keep alive for the long term. It comes down to a matter of money, ala Terri Schiavo or Christopher Reeve. The more money you have, the better you can do, but it's a losing game, and for people with no effective consciousness, usually one that nobody is willing to play. SBHarris 23:26, 16 January 2007 (UTC)
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- Since there is no "cure" for AD, everyone who has it will die with it, but not necessarily from it. It can cause death by shutting down brain function. I will get a source and description of that, but of course, "How we Die" by Sherwin Nuland is the classic. --Chrispounds 23:38, 16 January 2007 (UTC)
- I do not think you'll find a case of anybody dying of Alheimer's which had progressed to the point of shutting down brain stem function and causing classical brain death. It just doesn't work that way. Nor would anybody allow the process to go on that long, even if it did. SBHarris 23:41, 16 January 2007 (UTC)
- Since there is no "cure" for AD, everyone who has it will die with it, but not necessarily from it. It can cause death by shutting down brain function. I will get a source and description of that, but of course, "How we Die" by Sherwin Nuland is the classic. --Chrispounds 23:38, 16 January 2007 (UTC)
- Just to make it clear: People who develop Alzheimer's can live from 2 to 20 years with the disease, but Alzheimer's disease is a terminal illness. Due to the deterioration in the brain and body, a person becomes more susceptible to various complications, such as infection, that can cause death. While infection may be the immediate cause of death, the underlying cause is the deterioration brought about by AD. In the brain with Alzheimer's disease neurons continue to die over time and eventually the body will shut down. However, people usually die of secondary infection. It is usually not the actual Alzheimer's that ends a person's life, but rather, any one of a number of side effects of the disease. Such as influenza or pneumonia brought on by compromised immune system. --Igoruha 23:34, 17 January 2007 (UTC)
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- Yes, and you can say just the same about being a high level quadruplegic. Potato, potahto. Aging itself is a terminal illness. Nobody has died of old age since 1955 when they outlawed it as a cause of death to put on death certificates. Since then, it's been putting down "complications" only. Doesn't change reality. SBHarris 04:41, 17 January 2007 (UTC)
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- Thanks for your reply Igoruha. I would like to see such an explanation in the article. iyigun 17:04, 20 January 2007 (UTC)
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- AD is such a problem with memory that the person actually forget or don't take their medication for infections as an example. This is the cause of death in patients. They forget to pee, forget to do every day things. These are the causes secondary to AD. —The preceding unsigned comment was added by 69.43.113.2 (talk) 18:43, 4 April 2007 (UTC).
- therefore AD itself is not a killer disease, surely? it makes me wonder when people say, oh he died from AD. not possible! AD makes you forget, etc, but it does not stop the body from functioning, or does it? it's not terminal like MS or MND. 194.221.133.226 (talk) 12:29, 8 January 2008 (UTC)
Alzheimer's disease is a terminal condition that progressivly gets worse over time and is fatal. The first symptom is always deficits in memory followed by aphasia, apraxia, and agnosia after several years. Personality changes, increased irritability, and other behavioral changes can start in the early stages but become most pronounced in the middle stage. In the later stages gait and motor disturbances are common and increase the chance of physical injury because of coordination inabilitys. Also in the later stages individuals can become mute or bedridden. Individuals with Alzheimer's disease may become very vulnerable to physical and mental stressors increasing the risk of Illness and further mental deterioration. The disease severly damages the frontal lobe and associated subcortical pathways. The average amount of time from onset of symptoms to death is 8-10 years... thats quoting the DSM-IV TR.... Id also like to point out that your brain controls the functions that keep you alive. so its reasonable to say that if a disease were to damage parts of the brain that control essential functions your body will shut down. Also the fact that the frontal lobe is being damaged and the patient is loosing there mental abilitys I would think is unbearably stressful on the brain and body and something to that extreme can cause your brain to just give up and quit working. since AD damages the frontal lobe the risk of impaired motor, speech, and comprehension abilitys is almost guarenteed. It also can make patients forgot to preform nessecary things like exreting waste, personal hygene, when and what to eat... that could cause toxicity, sepsus, anemia, etc. and those conditions have high mortallity rates. Basically Individuals with AD will die either from an Illness, A medical condition related to side effects of AD, or simply from AD itself.JonM.D. (talk) 10:35, 10 January 2008 (UTC)
Aluminum
The Alzheimer's Association of the US has issued this fact sheet on aluminum. [1]. Given their scientific board of directors, I think this is enough evidence to remove Aluminum from the risk factor list. The Paquid study results are interesting, but the association's judgment seems to represent the broader opinion on the subject. The AAGP position statement does not mention aluminum. --Chrispounds 15:34, 26 April 2007 (UTC)
- Couldn't access the pdf today. There's a comment in this document from Alzheimer's Assoc. This also addresses it as "Myth 4". Without direct access to the article here but only the citation, I'm not inclined to continue including aluminum either, except perhaps as a caveat that it "was once believed" but now most researchers focus on other factors, considering the effects of regular aluminum use for consumable goods containers a non-concern. ZueJay (talk) 02:06, 3 August 2007 (UTC)
Do the objections above remind anyone of the Vatican vs Galileo? When a study showing a link between alzheimer's and aluminum intake has been peer-reviewed and published in the American Journal of Epidemiology, it deserves consideration as a possible risk factor. If the science is sound, it should not matter if Alzhemier's Association has not yet accepted it. The Aluminum industry's obvious objections not withstanding, the real scientists contributing to this article should be willing to consider challenges to the dominant paradigm. --senchang 01:02, 14 November 2007 (UTC)
- A special edition of the Journal of Alzheimer's described Aluminum as "especially controversial" [[2]] and thus does not meet the standards we have set with other risk factors as being generally accepted by the scientific community. --Chrispounds 14:34, 14 November 2007 (UTC)
I remeber reading an article at some point saying that aluminum cannot directly cause Alzheimers but that aluminum reaching the brain via blood can cause a build up of chemicals over time resulting in cognitive disfuction... —Preceding unsigned comment added by JonM.D. (talk • contribs) 10:45, 10 January 2008 (UTC)
- Sorry, but unless you've got a reference, it's just rumour. LeadSongDog (talk) 04:52, 31 January 2008 (UTC)
Pruning
The target article length for wikipedia is 50,000 characters and we are north of 62,000 as of this writing. I am working toward maintaining the sense of the article whilst trimming it down. One strategy would be to have someone prune and then others come in and copy edit. We also should get a little more tight with our references. Let's shoot for 85% medical references and try to get the primary source rather than a press release from the primary. --Chrispounds 00:46, 15 July 2007 (UTC)
- I'd rather not see any material lost. Looks to me like the 'pathology' section is too long, and a lot of that should go into the 'Biology of Alzheimers' main page
peterl 03:02, 7 August 2007 (UTC)
CF Research Links Protein, Stem Cells and Potential Alzheimer’s Treatment
Sugaya is now investigating whether a combination of phenserine and his compound (NBI-18), which increases brain stem cells by 600 percent, could become another way to treat Alzheimer’s. [3] [4] Brian Pearson 02:35, 7 August 2007 (UTC)
The owner of the compound had announced they were not continuing development because of failure in late stage trials. [5] Only late-stage (Phase 3) compounds have been listed to conserve space. --Chrispounds 11:05, 7 August 2007 (UTC)
Cannabis
There is much information on the internet about the use of cannabis to treat this disease, some of it is below
Cannabis lifts Alzheimer appetite - Thursday, 21 August, 2003,
The drug is an artificial version of a cannabis component A cannabis-based drug could help people with Alzheimer's disease by giving them the "munchies", researchers say.
http://news.bbc.co.uk/1/hi/health/3169901.stm
Marijuana may block Alzheimer's - Tuesday, 22 February, 2005,
The compound may protect the brain The active ingredient in marijuana may stall decline from Alzheimer's disease, research suggests.
http://news.bbc.co.uk/2/hi/health/4286435.stm
Cannabis may help prevent Alzheimer's memory loss
Ben Sills in Madrid and Ian Sample - Thursday February 24, 2005
http://www.guardian.co.uk/life/science/sto...1424013,00.html
Hope for cannabis-based drug for Alzheimer's - 18 October 2006
http://www.newscientist.com/channel/health/dn10330-hope-for-cannabisbased-drug-for-alzheimers.html
Science Daily — New evidence in rats suggests that marijuana may contain compounds that slow the memory loss associated with Alzheimer's disease.
October 18, 2006
2007-08-03
Marijuana May Slow Alzheimer's
THC, the key compound in marijuana, may also be the key to new drugs for Alzheimer's disease.
http://almost420.blogspot.com/2007/08/mari...-alzheimer.html JHJPDJKDKHI! 03:52, 9 August 2007 (UTC)
- Thank you for bringing this information to our attention. The fact that there are a lot of info about cannabis as in relation to AD just says that there are a lot of speculations on this topic, which does not necessarily mean that a credible scientific research has been done on that topic. So in the future, if you want to back up your claim please use scientific peer reviewed sources. That said, you are correct - cannabinoid receptor agonists are in deed effective at preventing amyloid-β toxicity as was reported by Milton in 2002 and 2005 (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&dopt=AbstractPlus&list_uids=15709490, http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&dopt=AbstractPlus&list_uids=12384227). As Professor Milton himself notes, "At higher doses, cannabis can have toxic effects themselves, and as a treatment, an effective dosing regimen is essential. A specific agonist without toxic or detrimental behavioral actions would be the ideal candidate; more investment may help develop such a compound.The future for cannabinoid therapy still needs investment to realize its true potential." So, research is being conducted on this topic, but it might be premature to list it as a reliable treatment option in one form or another. Igoruha 21:01, 10 August 2007 (UTC)
Vaccine thwarts the tangles of Alzheimer's
"It's likely that there's a synergism in the pathology," said Dr. Sigurdsson. "Amyloid pathology may cause tau pathology and tau pathology might cause more amyloid pathology. What you have is a vicious cycle. If you can target both of these proteins you'll likely have more efficacious treatment." [6] Brian Pearson 22:40, 21 August 2007 (UTC)
Copper and Alzheimers ?
Copper and Alzheimers ?
Months ago, I listed a discovery of discovered link between copper and Alzheimers. Dr. Rosanna Squitti, today, her listing is being reviewed for deletion, and upon review of Alzheimers, the discovery of her discovery is not there ?
Is there a political agenda to elminate any reference between Alzheimers and heavy metals ?
--Caesar J. B. Squitti : Son of Maryann Rosso and Arthur Natale Squitti 17:18, 4 September 2007 (UTC)
- The issue is scientific and not political. Why are you suggesting this is political? Late stage development of heavy-metal compounds has not shown success in treating Alzheimer's. Animal based models are not sufficient scientific proof for the inclusion on this page. The major US Alzheimer's Association has completely discounted the aluminum theory and does not mention copper. Find a major longitudinal epidemiologic study from recent years that lists copper as a risk factor. --Chrispounds 12:11, 12 September 2007 (UTC)
I would like to suggest that any substance that is neurotoxic while perhaps not a cause of Alzheimers may hasten its effects. Copper I believe is a neurotoxin. Related to this is the possibility that Alzheimer's may affect the brains ability to deal with neurotoxins. In the case of copper, for example, even if in a non-Alzheimer's subject, copper does not affect cognition, it may be possible that the Alzheimer's brain is unable to remove/handle copper as effectively and therefore we see cognitive effects which is of course added to the effects caused by the disease itself.
Perhaps substances that are not identified as neurotoxins at all can become neurotoxic in Alzheimer's.
Mercury and lead, which definitely affect cognition, may be especially dangerous to Alzheimer's patients.
I hope this idea will result in further discussion.--Jrm2007 (talk) 07:15, 12 May 2008 (UTC)
- Sounds like original research. If you can find some reliable sources, please add it to the article. Otherwise, it doesn't belong here. OrangeMarlin Talk• Contributions 07:59, 12 May 2008 (UTC)
No, it is not original research. I am not suggesting putting it in the article -- I think it is acceptable to have such ideas in the discussion page, no?Jrm2007 (talk) 08:39, 12 May 2008 (UTC)
Alzheimer disease: type of dementia?
"It is the most common type of dementia."
This claim, which occurs several times in the article, is flawed. Dementia is a syndrom and is only one part of the Alzheimer disease. Even more, there are three types of dementia in Alzheimer disease. See http://www.mentalhealth.com/icd/p22-or04.html
--Eleassar my talk 12:26, 21 September 2007 (UTC)
- I note that the change from "most common cause of dementia" to "most common type of dementia" was done by an anon editor who has made no other edits, at 11.17 on 22 Oct 06. Is that really right? PamD 22:57, 23 September 2007 (UTC)
- The epidemiological presentations I recall have reported that the of patients with dementia, dementia of the Alzheimer's type is the most common in these patients. I believe that even counting mixed type (Alzheimer's and vascular, or AD and Dementia with Lewy Bodies, or Fronto-temporal dementia) as a pool, the AD population would be the most common. The Alzheimer's Association in the US makes this claim. [see http://www.alz.org/alzheimers_disease_what_is_alzheimers.asp] The ICD-10 classification reflects a European bias. "Dementia of the Alzheimer's type" is how most in the US describe it (see clinicaltrials.gov), although some have talked about relabeling the disease "Alzheimer's dementia" to more closely link the concept that Alzheimer's disease is a dementia. --Chrispounds 23:21, 23 September 2007 (UTC)
- Fair enough. The (UK) Alzheimer's Society at [7] says "There are over 100 different types of dementia. The most common are Alzheimer’s disease, vascular dementia and dementia with Lewy bodies.". That's good enough for me! I'd previously thought the dementia was the the effect rather than the disease, but was wrong. Even anon editors with no other edits can be right! PamD 07:24, 24 September 2007 (UTC)
What bothers me here is the distinction between Alzheimer's disease and Alzheimer's dementia (a disease and a syndrom). One cannot define signs and symptoms as a disease per se. There are biochemical and histological changes as well. Even more so as even not counting mixed type dementia there are still two types of clinical presentation/dementia in AD: early onset and late onset. --Eleassar my talk 09:28, 24 September 2007 (UTC)
- I see you believe that you need to see underlying biophysical changes to believe that as disease is present, but practically in Alzheimer's disease this is not how it is being diagnosed. Only about 1/3 of US physicians do imaging before giving the Alzheimer's diagnosis--and this is for rule-out diagnosis rather than rule-in. The new European guidelines from EFNS look for confirmation with biochemical data see PMID: 17222085, but not everyone will practice according to the guidelines. Also from EFNS, a researcher from Antwerpen presented data that showed that CSF biomarkers taken pre-mortem in 50 AD patients did not correlate with post-mortem pathology. Clinical trials of products have also shown changes in biomarkers (hippocampal volume) that give significant results but the clinical signs are not significant. Functional neurological disorders also have the problem of missing underlying pathology, but does this mean they do not exist?
- We have presented two sources that state AD as the most common form of dementia. My reading of the WHO/ICD-10 does not dispute this but rather points to some semantical differences. Would you agree? --Chrispounds 15:32, 25 September 2007 (UTC)
Yes, thanks for having pointed this out. So it would be more appropriate to call this entity Alzheimer's dementia and the article should not describe it as a disease but as a syndrome (after all, its etiology is unknown)? --Eleassar my talk 17:43, 25 September 2007 (UTC)
- I think the present belief that the hallmarks of disease on the pathophysiological side (plaques and tangles) are associated with the clinical signs and symptoms (cognitive loss, loss of ADLs) still stands up and that Kraeplin was correct in calling it Alzheimer's disease. The label of Alzheimer's disease is what is commonly used for what may be a syndrome--although the genetics suggest that amyloid is in the cascade of the etiology. But, if you look in the literature for "alzheimer's syndrome," the 13 pubmed articles are not going to justify the 65k article we have. This dispute seems to have been won by the "disease" camp--at least based on usage in the scientific literature. Rebranding a disease (Lou Gehrig to ALS) is a very long row to hoe. --Chrispounds 04:36, 26 September 2007 (UTC)
Perhaps it would be more appropriate and more neutral to define it as a disorder rather than a disease. Anyway, I have removed the disputed tag now. --Eleassar my talk 10:16, 26 September 2007 (UTC)
- I think it is most appropriate to use the language that everyone has been using for the last 90+ years for it: Alzheimer's disease. This is how the medical literature refers to it and this is how the public talks about it. Perhaps semantically it is really something slightly different and does not fit a specific definition. This makes one wonder if the definition of disease is something that needs to be changed and not this name (AD). I will let the editors on that talk page discuss that. --Chrispounds 13:28, 27 September 2007 (UTC)
- It's certainly a disease if any disease is a disease. Disorders are things with no recognized pathology, like conduct disorder. Or with no unifying pathology like dementia or schizophrenia. But AD has characteristic histopathology. Early diseases may have no syndrome (set of clinical SYMPTOMS), and AD is no exception. It's like high blood pressure or diabetes in that regard: when starting out, you may not know you have it. But the disease is not the symptoms. Dementia is a syndrome, a set of symptoms, like shortness of breath. It's not itself a disease. If you think of "dementia" as shortness of breath, and AD as being like "emphysema" you'll have a good analogy. AD is only one of a number of dementing illnesses, but early AD does not yet sometimes cause dementia, or may cause it only under stress, just as early emphysema may not cause shortness of breath, or only cause it under stress.
BTW, the term "Alzheimer disease" (no apostrophe or s) is actually more common in the scientific literature of the present day, which you can verify by typing it into medline and looking at paper titles. This probably should be the name of the article, with a redirect from "Alzheimer's disease." SBHarris 20:34, 30 October 2007 (UTC)
- I think Neurology has moved to Alzheimer disease, but NEJM, Nature, and Science are not consistent with Alzheimer's. The ICAD meeting which is the largest meeting for AD still calls it Alzheimer's disease. I would keep it for now until the scientific community is consistent. --Chrispounds 14:29, 13 November 2007 (UTC)
- Chris, the very fact that there is great inconsistancy out there means it's necessary to keep both terms in the article. I'm willing to compromise on the article name, but I strongly object to removing all mention of Alzheimer disease in the article AT ALL. If you go to PUBMED and read the papers on the subject, (you get the same list of course no matter which term you use to search), then look at the TITLES of the papers, you'll see that Alzheimer disease wins. The scientific community has therefore spoken as well as it can to the issue of concensus. You've got the article titled with a minority term insofar as recent research. SBHarris 17:52, 17 November 2007 (UTC)
- I think Neurology has moved to Alzheimer disease, but NEJM, Nature, and Science are not consistent with Alzheimer's. The ICAD meeting which is the largest meeting for AD still calls it Alzheimer's disease. I would keep it for now until the scientific community is consistent. --Chrispounds 14:29, 13 November 2007 (UTC)
- It's certainly a disease if any disease is a disease. Disorders are things with no recognized pathology, like conduct disorder. Or with no unifying pathology like dementia or schizophrenia. But AD has characteristic histopathology. Early diseases may have no syndrome (set of clinical SYMPTOMS), and AD is no exception. It's like high blood pressure or diabetes in that regard: when starting out, you may not know you have it. But the disease is not the symptoms. Dementia is a syndrome, a set of symptoms, like shortness of breath. It's not itself a disease. If you think of "dementia" as shortness of breath, and AD as being like "emphysema" you'll have a good analogy. AD is only one of a number of dementing illnesses, but early AD does not yet sometimes cause dementia, or may cause it only under stress, just as early emphysema may not cause shortness of breath, or only cause it under stress.
Accourding to the DSM-IV-TR Alzheimers disease is a form of dementia. Other kinds of dementia include vascular dementia, dementia due to HIV, Dementia due to head trauma, Dementia due to Parkinson's, Huntington's, Pick's, and Creutzfeldt-jakob disease, substance induced dementia, and dementia due to multiple etiologies. Alzheimers is a type of dementia but demenitia is not a type of alzheimers disease. also many nuerological disorders could be considered a mental disordor and a medical condition... i.e. Somatoform disorders —Preceding unsigned comment added by JonM.D. (talk • contribs) 10:59, 10 January 2008 (UTC)
Article is too long
Although we have a lot of interesting sections, I believe the target length is around 50k for this article and we are around 64k. I would cut down Alzheimer's in the media and perhaps try to prune some of the potential treatments down now that the scene there is changing. Any other places where we could trim and still be coherent. Because the clinical stuff tries to keep to things that are active in the current practice, I would propose cutting out the section on diagnosis via the eyes until that has been validated. We could bring up blood based tests or some of the MCI screens out there in a separate section on testing for Alzheimer's disease. --Chrispounds 14:10, 30 October 2007 (UTC)
I agree the article is too long. At the same time much of the information could be reordered in a beter way. I think there are also some inaccuracies and a lack of citations. Maybe the article and subarticles on Multiple sclerosis could be used as an example to improve it. (Therapies for multiple sclerosis, Pathophysiology of multiple sclerosis...). I´ll try to help but as many of us I have a lack of time and much to do both in wikipedia and real life. --Garrondo 15:23, 5 November 2007 (UTC)
- Out of interest, where does it say the target length is 50K? --Matt Lewis (talk) 13:11, 14 January 2008 (UTC)
- As I recall, when you finished an edit it would report the length of the article and it would report that the article was longer than 50k and it recommended shortening it. This may have been removed--I have not noticed it. But as an encyclopedia entry, we should be concerned about length of the base article. --Chrispounds (talk) 14:26, 14 January 2008 (UTC)
- See Wikipedia:Article size --Chrispounds (talk) 14:54, 14 January 2008 (UTC)
A first and small simplification proposal-Diagnosis
The brain imaging and eye analysis paragraphs in the diagnosis part are superfluous: The first becouse Spect is alredy mentioned before and it talks about brain imaging in general and not related to AD; the second becouse the article mentioned is basic investigation, not applyable yet to clincal practice, also the conclusions given in the EA article are almost original research since they are not even mentioned in the abstract of the article about eye analysis. If not contested in the following days I will procceed to eliminate them. --Garrondo 14:13, 6 November 2007 (UTC)
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- They aren't superfluous now. SPECT and PET are as good at diagnosis of AD as are mental exams, yet the article only mentions them peripherally as confirmatory and differentiating tests. In the real world of medicine, that's not how they're used at all. In medicine, you can diagnose a probable non-displaced bone facture by the pain, swelling, and history. But if you want to tell exactly how bad it is, you use X-ray. Similarly, dementia is a clinical diagnosis, but if you want to know if it's caused by AD, without doing an autopsy or biopsy, you use PET and/or SPECT. This is far more a clinical standard than many of the treatments and putative risk-reducer for the disease, as mentioned below. And yet the information has been more or less deleted from from previous article versions. SBHarris 05:17, 18 November 2007 (UTC)
- One of the standards we tried to set in earlier revisions is that the information and research presented should not be novel nor cutting-edge but rather generally accepted in clinical practice. The treatment and potential treatments were only for approved or Phase 3 compounds, so we may need to do some pruning. Risk reducers should also be supported by large epidemiological evidence or a statistically significant clinical trial in humans. --Chrispounds 15:02, 6 November 2007 (UTC)
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- The October issue of Alzheimer's and Dementia has some great review articles by Canadian authors that captures a bunch of the latest research thinking. We might want to use some of these articles to sort through some of the Risk factors. --Chrispounds (talk) 22:27, 4 December 2007 (UTC)
From now on
I think this article right now is a good article. Nevertheless I feel much has to be done if it wants to become a Featured article in the future. Right now I feel its worse problem is the lack of proper scientific citations. This complicates a lot the verification of some of the data, and therefore it makes really hard to know what is important enough to stay and what should be moved to secondary pages or even eliminated. My proposal would be that we attacked each section one by one begining from the top to the botton looking for citations in peer-review journals and verifying all the info. In this way by the time we get to the less ordered parts of the article (lasts sections) much of the work would be already done. Garrondo 14:29, 13 November 2007 (UTC)
- Okay, I'm going to begin by adding a couple of citations suggesting that functional neuroimaging is as good at diagnosing AD as clinical tests, and better at differentiating it from other types of dementias. SBHarris 08:04, 18 November 2007 (UTC)
- I have finished revising the diagnosis section. I have added some new info; but specially I have fully referenced the section (almost 15 new references). All this has made the section a bit longer but I believe the results are worth it. I was thinking of adding a picture. Can anybody get a public domain PET or SPECT image of an Alzheimer patient (I was thinking of somebody working in a hospital...). There aren't any in commons. The next section I will try to improve is the clinical course since it also has an important lack of citations. The Pathology section is fully referenced; however it would be very interesting to try to writte a plain language summary to introduce the section, since the info it gives is from my point of view to much specific and complicated for those who are not familiar with biological terms. Can anybody do it?--Garrondo (talk) 17:07, 9 December 2007 (UTC)
Smoking
It's quite clear from Anstey KJ, von Sanden C, Salim A, O'kearney R (2007). "Smoking as a risk factor for dementia and cognitive decline: a meta-analysis of prospective studies". Am. J. Epidemiol. 166 (4): 367-78. doi:10.1093/aje/kwm116. PMID 17573335. and http://news.bbc.co.uk/1/hi/health/2994304.stm that smoking itself is not a risk reducer in Alzheimers. For the print document, please quote relevant text here. Please don't revert without discussion. peterl (talk) 03:13, 13 December 2007 (UTC)
- Yes. The idea that smoking is protective is from older case-control studies, and has been pretty much overturned by better epidemiology. Interestingly, it's harder to prove that smoking has any effect on APOepsilon4 carriers-- the folk who have the much higher risk of AD anyway. Smoking seems to hurt non-APOε4 carriers worse: PMID 9652667 SBHarris 03:59, 13 December 2007 (UTC)
- Conversely, is there anything published on forgetting to have a smoke as a cure for the addiction? LeadSongDog (talk) 04:57, 31 January 2008 (UTC)

