Talk:Apolipoprotein E

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SNP Positions[edit]

The positions to determine E2/E3/E4 were listed as 112 and 158, but dbSNP had the positions in the reference paper as 130 and 176, I changed the page accordingly, not sure where this discordance came from... —Preceding unsigned comment added by 140.247.90.36 (talk) 22:21, 21 February 2011 (UTC)[reply]

I just made the reverse change. Perhaps there are two numbering systems (both my version and the previous one list two positions separated by 46 base pairs). OMIM and the two scientific articles cited (Zuo et al 2006, Ghebranious et al 2005) list the positions as 112 and 158, so I aligned Wikipedia with those. I'm new to Wikipedia editing so apologies if I'm violating any conventions here. Emjonaitis (talk) 13:34, 6 April 2011 (UTC)[reply]

The discrepancy between the two notations arises because of a precursor peptide that is often included in the protein sequence that is commonly cleaved after expression. Therefore, the amino acid positions are usually counted without the precursor peptide (112 and 158). User:AS

Cardiac risk[edit]

PMID 17878422 - meta-analysis of coronary risk. JFW | T@lk 07:37, 23 September 2007 (UTC)[reply]

E2 allele[edit]

The article states that E2 is associated with hyperlipoproteinemia. According to Stearns & Koelle "Evolution in health and disease" p. 306 "only a small fraction (<5%) of E2 homozygotes develops a rare lipoprotein disorder (type III HLP), which involves elevated plasma cholesterol and TAGs...." --Padder333 (talk) 16:47, 3 March 2010 (UTC)[reply]

Suggested removals[edit]

The statement "Some ApoE4 homozygotes never develop the disease." might be a little misleading. As I understand it, this population is vanishingly rare among homozygotes who survive to old age. — Preceding unsigned comment added by 128.163.7.131 (talk) 20:03, 19 July 2012 (UTC)[reply]

From Function section: "Neonates with brain injuries and/or defects who also have abnormalities in the APOE gene may have an increased risk for cerebral palsy, according to researchers at the Northwestern University Feinberg School of Medicine[citation needed]." This is not referenced and there are literally thousands of studies with other random findings that we could just as easily place here. It is not clear that this study is particularly representative of APOE —Preceding unsigned comment added by 165.124.163.251 (talk) 21:45, 31 December 2010 (UTC)[reply]

"Epistatic impact of APOE

Apolipoprotein A-I and APOE interact epistatically to modulate triglyceride levels in Coronary Heart Disease patients.Individually, neither ApoA-I nor ApoE was found to be associated with TG levels however, pairwise epistasis (additive x additive model) explored their significant synergistic contributions with raised TG levels (P<0.01).[12]"

I am removing this entire section. These types of findings can be notoriously difficult to replicate, and unless it has been replicated and there are wider implications to this study which our general audience might be interested in, it doesn't seem worth the distraction. Also, not sure we really need to be reporting p values here unless it addresses particularly contentious issues.Pengortm (talk) 01:05, 1 January 2011 (UTC)[reply]

Just removed this section as well because I think it spends too much time on an area that clearly is not well established, and is probably not that important to the larger article:

Among ApoE4 carriers, another gene, GAB2, is thought to further influence the risk of getting AD.^[1] However, the relationship does not appear as strong as e4, since in the Japanese population, gab2 is not a risk factor. More recent work questions this effect, since GAB2 does not seem to modify AD risk in e4 carriers in the Spanish population. ^[2] Pengortm

^ Reiman EM, Webster JA, Myers AJ, Hardy J, Dunckley T, Zismann VL, Joshipura KD, Pearson JV, Hu-Lince D, Huentelman MJ, Craig DW, Coon KD, Liang WS, Herbert RH, Beach T, Rohrer KC, Zhao AS, Leung D, Bryden L, Marlowe L, Kaleem M, Mastroeni D, Grover A, Heward CB, Ravid R, Rogers J, Hutton ML, Melquist S, Petersen RC, Alexander GE, Caselli RJ, Kukull W, Papassotiropoulos A, Stephan DA (2007). "GAB2 Alleles Modify Alzheimer's Risk in APOE varepsilon4 Carriers". Neuron. 54 (5): 713–720. doi:10.1016/j.neuron.2007.05.022. PMC 2587162. PMID 17553421.{{cite journal}}: CS1 maint: multiple names: authors list (link) Free full text Free PDF Genetic data in the public domain
^ Ramirez-Lorca R; et al. (2009). "GAB2 gene does not modify the risk of Alzheimer's disease in Spanish APOE 4 carriers". J Nutr Health Aging. 13 (3): 214–9. PMID 19262956. {{cite journal}}: Explicit use of et al. in: |author= (help)

Statins and Alzheimer disease[edit]

There is some evidence that statins are protective against dementia.[1] Alzheimers is not listed as a side effect for the two statins I checked.[2][3] Can the claim that AD is an adverse effect of statins really be supported?BiologicalMe (talk) 15:07, 27 August 2014 (UTC)[reply]

None of the references supported the claim, and the material was deleted.BiologicalMe (talk) 12:25, 15 September 2014 (UTC)[reply]

External links modified[edit]

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Women vs. men?[edit]

I can't find word WOMEN in Wikipedia article so I suppose sex differences are not discussed.

"Women are more likely to develop AD=Alzheimer disease than men across most ages and APOE genotypes. Women with the APOE ε3/ε4 genotype are at approximately 4-fold increased risk. Men with it show little to no increased risk".

http://www.jneurosci.org/content/32/24/8254

ee1518 (talk) 15:20, 17 November 2017 (UTC)[reply]

COVID-19 and APOE epsilon 4[edit]

This is statement that APOE e4 is associated with everything bad about Covid-19 (in the disputed section)is based on only ONE very early study has not even been replicated. In fact, this study is controversial and disputed. See https://www.sciencemediacentre.org/expert-reaction-to-study-on-covid-19-and-a-faulty-gene-linked-to-dementia/. Indeed, APOE4 is typically protective against infections because of the robust immune defenses, so this study seems dubious. This is just one example of how insufficient research or unsubstantiated statements and assumptions about this APOE isoform are being distorted. It seems like it has deteriorated to just throwing everything at the APOE4 wall to see what sticks.

APOE ε4 and telomere length[edit]

The claim is made in this article (in the disputed section) that APOE ε4 is associated with shortened telomere length or accelerated telomere shortening, and that the shortened telomeres are pathogenic (the article cited is a single study with novel presumptions and findings, and never replicated). This is a highly misleading claim the way it is stated, as it generalizes from very specific issue and population (older women on hormone therapy). You can't take one very narrow unreplicated study and apply it to everyone. If you want to discuss the narrow implications of how hormone therapy might mitigate telomere characteristic, fine. But do it in a separate article, not a general article on APOE. There are many other studies that show that APOE ε4 is associated with longer telomere length, with the longer telomere also being pathogenic, such as this article: Wikgren M, Karlsson T, Nilbrink T, Nordfjäll K, Hultdin J, Sleegers K, Van Broeckhoven C, Nyberg L, Roos G, Nilsson LG, Adolfsson R, Norrback KF. APOE ε4 is associated with longer telomeres, and longer telomeres among ε4 carriers predicts worse episodic memory. Neurobiol Aging. 2012 Feb;33(2):335-44. doi: 10.1016/j.neurobiolaging.2010.03.004. Epub 2010 Apr 14. PMID: 20395015.

First, I would say calm down, and remember WP:Assume good faith. It seems like you're right, and I've updated the article accordingly, and removed the disputed content banner. Please sign your comments in the future. -- SoloBear89 20:24, 29 June 2022 (UTC)[reply]

[1] Reiman EM, Webster JA, Myers AJ, Hardy J, Dunckley T, Zismann VL, Joshipura KD, Pearson JV, Hu-Lince D, Huentelman MJ, Craig DW, Coon KD, Liang WS, Herbert RH, Beach T, Rohrer KC, Zhao AS, Leung D, Bryden L, Marlowe L, Kaleem M, Mastroeni D, Grover A, Heward CB, Ravid R, Rogers J, Hutton ML, Melquist S, Petersen RC, Alexander GE, Caselli RJ, Kukull W, Papassotiropoulos A, Stephan DA (2007). "GAB2 Alleles Modify Alzheimer's Risk in APOE varepsilon4 Carriers". Neuron. 54 (5): 713–720. doi:10.1016/j.neuron.2007.05.022. PMC 2587162. PMID 17553421.{{cite journal}}: CS1 maint: multiple names: authors list (link) Free full text Free PDF Genetic data in the public domain

[2] Ramirez-Lorca R; et al. (2009). "GAB2 gene does not modify the risk of Alzheimer's disease in Spanish APOE 4 carriers". J Nutr Health Aging. 13 (3): 214–9. PMID 19262956. {{cite journal}}: Explicit use of et al. in: |author= (help)

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