Submited on: 15 May 2014 06:28:11 PM GMT
Published on: 16 May 2014 04:44:12 AM GMT
 

  • What are the main claims of the paper and how important are they?

    Keywords should be consultd in NLM-Mesh to verify IF they are accepted:

    http://www.nlm.nih.gov/mesh/MBrowser.html


  • Are these claims novel? If not, please specify papers that weaken the claims to the originality of this one.

    Introduction, 2nd paragrapgh: “Both the antiapoptotic effect of n-3 PUFA and Akt translocation are sensitive to n-3 PUFA-induced PS accumulation, strongly suggesting that the antiapoptotic effect of n-3 fatty acids depends on its ability to accumulate PS in neuronal membranes. The ability of dietetic ?sh oil to nullify the age-dependent disturbances of the PS turnover as well as hippocampus function suggests the critical PS role in cognitive function decline during normal physiological aging.” This sentence does not contain reference, it should be included.


  • Are the claims properly placed in the context of the previous literature?

    Introduction, the authors should remove the following paragraph: “In the present paper a significant increase of the newly synthesized PS  content has been observed in the hippocampus of alpha-tocopherol-treated 24-month-old rats. Alpha-tocopherol could ameliorate the age-dependent decline of cognitive function of old animals. Manipulating of the PS level in the hippocampus of the aged animals with alpha-tocopherol may be a strategy for improvement learning and memory abilities.” This is because the paragraph presents similar content of the above paragraph.


  • Do the results support the claims? If not, what other evidence is required?

    Method, Behavioral  Characteristics  of Experimental Animals: The mentioned protocol was already used in another study? If positive, please, cite it in the reference.


  • If a protocol is provided, for example for a randomized controlled trial, are there any important deviations from it? If so, have the authors explained adequately why the deviations occurred?

    Method, Statistical analysis: Was it applied normality test? Which one was applied? Kolmorogov-Smirnov?


  • Is the methodology valid? Does the paper offer enough details of its methodology that its experiments or its analyses could be reproduced?

    Method, Statistical analysis: The authors mentioned that Newman–Keuls test was applied. Please, confirm wheather the ANOVA oneway test was applied.


  • Would any other experiments or additional information improve the paper? How much better would the paper be if this extra work was done, and how difficult would such work be to do, or to provide?

    Results and Discussion should be divided in separated topics.


  • Is this paper outstanding in its discipline? (For example, would you like to see this work presented in a seminar at your hospital or university? Do you feel these results need to be incorporated in your next general lecture on the subject?) If yes, what makes it outstanding? If not, why not?

    Results should present Tables or Figures to illustrate the author’s findings


  • Other Comments:

    Discussion should begins with a summary of the main findings.

  • Competing interests:
    None
  • Invited by the author to review this article? :
    Yes
  • Have you previously published on this or a similar topic?:
    No
  • References:

    None

  • Experience and credentials in the specific area of science:

    Cardiovascular physiology

  • How to cite:  Valenti V E.Review on Vitamin E stimulates phosphatidylserine synthesis in the hippocampus and improves cognitive function at old age [Review of the article 'Vitamin E stimulates phosphatidylserine synthesis in the hippocampus and improves cognitive function at old age ' by Hassouneh L].WebmedCentral 2014;5(7):WMCRW003080
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  • What are the main claims of the paper and how important are they?

    The paper suggests that Vitamin E alters phospholipid synthesis in the hippocampus that is associated with increased cognitivie function. There is an interesting result.


  • Are these claims novel? If not, please specify papers that weaken the claims to the originality of this one.

    There have been scores of papers linking dietary supplements, including antioxidants, to gains (and losses) in cognition.  Indeed, there are several hundred concerning the effect of Vitamin E alone.  However, this paper attempts to provide a direct mechanistic link between phospholipid synthesis, vitamin E and cognition which is novel.


  • Are the claims properly placed in the context of the previous literature?

    Yes. As noted, there is evidence for an effect of Vitamin E on cognition in various models, and the claims presented are in line with these earlier studies.


  • Do the results support the claims? If not, what other evidence is required?

    Although there is data indicating differences in cognition, as well as phospholipid synthetic pathways, these data do not appear to be from the same individuals.  In fact, the phospholipid data appears to have been generated using an in vitro system. Hence, this is a correlative paper at best.  It would have been stronger if vitamin E fed rats were subjected to cognitive tests before and after feeding, then hippocampi removed and phosphlipid levels determined. These measures could have also included measures of synthetic pathways post-mortem with the reasonable presumption that observed differences (if any) would have existed in intact animals.


  • If a protocol is provided, for example for a randomized controlled trial, are there any important deviations from it? If so, have the authors explained adequately why the deviations occurred?

    There is no specific protocol provided and the data itself may have not been analyzed properly. Specifically, there is no rationale provided for why one test bersus another was chosen, including a parametric test in one case and a non-parametric test in another.  There are also some concerns that a key assumption (equal variance) was violated in the data using the parametric test since there are no error bars for the controls.


  • Is the methodology valid? Does the paper offer enough details of its methodology that its experiments or its analyses could be reproduced?

    There are design flaws, especially the quantification of cognition and hippocampal phospholipid measures from different animals (see above) and using in vitro assays post-mortem in isolated tissues to draw inferences about what may have occurred in intact animals.  It sounds like the rats were given vitamin E/corn oil via gavage, but it is not explicitly stated.  Details concerning the sex, strain and supplier of the rats is missing. Details on diet are also lacking, especially whether or not the diets were isocaloric as this could influence cognitive measures if one was restricted versus the other; weight data would also help address this issue. A young control group is critical to be sure cognition is impaired in the older rats using the measures presented.  Presumably the cognitive measures were based on the ability of the rats to "learn" the task during the training, but it's unclear if this was so; also, what was the training for if this was the actual measure? Were the tisse samples used for the phospholipid assays slices? Lysates? Punches? Something else?


  • Would any other experiments or additional information improve the paper? How much better would the paper be if this extra work was done, and how difficult would such work be to do, or to provide?

    There is a fair amount of speculation concerning the mechanistic basis for the observed differences in PC content, but there are not data supporting/refuting these claims.  Measures of enzymes activites could have been included.  The hippocampal data are simply point measures as well, making it impossible to speculate on the activity of specific degredative/synthtic pathways. For example, if I understand the base exchange model properly, the label would need to be incorporated into PC first, then used as a substrate for the enzyme.  Likewise, if PC is being differentially degraded then determining how much of the label is incorporated (the measure reported) doesn't really provide a measure of PC degredationunless it was known with certaintly that loss of PC:gain of the label occurs in exactly a 1:1 ratio.


  • Is this paper outstanding in its discipline? (For example, would you like to see this work presented in a seminar at your hospital or university? Do you feel these results need to be incorporated in your next general lecture on the subject?) If yes, what makes it outstanding? If not, why not?

    The paper is interesting, especially given the apparent (and dramatic) differences in cognitive measures.  However, one of the purported strengths of the paper, namely that this is a result of differential phospholipid metabolism, is tenuous at best. As noted, there are more questions than answers, and the data are merely associative. 


  • Other Comments:

    No

  • Competing interests:
    None
  • Invited by the author to review this article? :
    Yes
  • Have you previously published on this or a similar topic?:
    No
  • References:
    None
  • Experience and credentials in the specific area of science:

    I have reviewed extensively on the role/effect of diet on aging parameters in diverse animal models for Aging Cell, Neurobiology of Aging and the American Journal of Physiology

  • How to cite:  Harper J .Review on Vitamin E stimulates phosphatidylserine synthesis in the hippocampus and improves cognitive function at old age [Review of the article 'Vitamin E stimulates phosphatidylserine synthesis in the hippocampus and improves cognitive function at old age ' by Hassouneh L].WebmedCentral 2014;5(6):WMCRW003078
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