A team of scientists have shown that the brains of patients with schizophrenia have the capacity to reorganize and fight the illness. This is the first time that imaging data has been used to show that our brains may have the ability to reverse the effects of schizophrenia.
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Guo, S., Palaniyappan, L., Liddle, P., & Feng, J. (2016) Dynamic cerebral reorganization in the pathophysiology of schizophrenia: a MRI-derived cortical thickness study. Psychological Medicine, 1-14. DOI: 10.1017/S0033291716000994
Have you read this sentence before? Perhaps it feels strangely familiar? The experience of déjà vu is a common one, but in rare cases, it can become a disorder. In a fascinating new Cortex paper, French psychologists Julie Bertrand and colleagues discuss the phenomenon of pathological déjà vu.
Bertrand et al. present an English translation of what is probably the first description of the condition, published in 1896 in French by the psychiatrist Francois-Léon Arnaud (1858-1927).
Ar... Read more »
Bertrand JM, Martinon LM, Souchay C, & Moulin CJ. (2016) History repeating itself: Arnaud's case of pathological déjà vu. Cortex; a journal devoted to the study of the nervous system and behavior. PMID: 27188828
It's another research mash-up today as I bring to your attention two papers talking about potential correlates associated with psychosis and/or psychotic symptoms.First up are the findings reported by Joanne Newbury and colleagues  (open-access here) who observed that urban residency and certain factors associated with urban residency might link into a higher risk of childhood psychotic symptoms. A second paper by Tomasz Pawełczyk and colleagues  provides some further food for thought and the suggestion that "dietary patterns of PUFA [polyunsaturated fatty acids] consumption may play a role in the conversion to psychosis of HR [ultra high-risk] individuals."Newbury et al report findings from the Environmental Risk (E-Risk) Longitudinal Twin Study and specifically the idea of "whether specific features of urban neighborhoods increase children's risk for psychotic symptoms." Aside from finding a potential association between urban residency at aged 5 and aged 12 and psychotic symptoms at aged 12, researchers also suggested that: "Low social cohesion, together with crime victimization in the neighborhood explained nearly a quarter of the association between urbanicity and childhood psychotic symptoms after considering family-level confounders."Pawełczyk et al continued a research theme suggesting that what we do or do not eat might have implications for some with regards to transition to psychosis (see here). Focusing specifically on a group of HR individuals, they looked at the diet of those who did and did not transition into psychosis. They reported: "C-HR [converted into psychosis] individuals reported significantly higher consumption of n-6 fatty acids (linoleic acid, LA and arachidonic acid, AA) in comparison with individuals who did not develop psychosis (NC-HR)."Although not seemingly covering the same factors when it comes to psychosis/psychotic symptoms, one of the things that I thought might also unite both these findings is food. Yes, Pawełczyk et al already talk about food (albeit based on the warts and all use of "a validated Food-Frequency Questionnaire") but the Newbury paper might also include a food element insofar as what types of food might be more readily available and eaten in urban vs. not-so-urban environments.Bearing in mind that sweeping generalisations about food availability and importantly, what types of food are available depending on where one lives, are not required, I would like to suggest that spatial patterning of say, supermarkets vs. fast food outlets might be something that could potentially unite results. The paper by Lamichhane and colleagues  for example found that: "the availability of supermarkets and fast food outlets differed significantly by neighborhood characteristics; neighborhoods with supermarkets and with fast food outlets were significantly higher in socio-economic status." Research looking at the causes and/or drivers of obesity have tended to predominate in the area of how neighbourhood might influence eating patterns  but similar modelling could be done with more psychiatric outcomes in mind. Indeed to quote Newbury et al: "Neighborhood-level physical exposures such as noise, light, and air pollution, as well as exposure to viral infections warrant research in relation to early psychotic symptoms." Who says that food should not also be included?I don't want to gloss over just how complicated the factors might be bringing someone to clinically relevant psychotic symptoms nor to say that food is somehow the 'missing' element for all cases. But it's not outside of the realms of possibility that in these days of nutritional psychiatry, food might exert an important effect for some people and food availability (certain food availability) could be one factor contributing to the idea that where you live might affect your risk of psychosis...And if that wasn't enough speculating, how about sweeping generalisations about maternal smoking habits and prenatal nicotine exposure as a risk factor for psychosis+  as something else potentially linked to urban living?---------- Newbury J. et al. Why are Children in Urban Neighborhoods at Increased Risk for Psychotic Symptoms? Findings From a UK Longitudinal Cohort Study. Schizophr Bull. 2016 May 6. pii: sbw052. Pawełczyk T. et al. The association between polyunsaturated fatty acid consumption and the transition to psychosis in ultra-high risk individuals. Prostaglandins Leukot Essent Fatty Acids. 2016 May;108:30-7. Lamichhane AP. et al. Spatial patterning of supermarkets and fast food outlets with respect to neighborhood characteristics. Health & place. 2013;23:10.1016/j.healthplace.2013.07.002. Macdonald L. et al. Neighbourhood fast food environment and area deprivation—substitution or concentration? Appetite. 2007; 49: 251-254. Niemelä S. et al. Prenatal Nicotine Exposure and Risk of Schizophrenia Among Offspring in a National Birth Cohort. American Journal of Psychiatry. 2016. May 24.----------Pawełczyk, T., Trafalska, E., Kotlicka-Antczak, M., & Pawełczyk, A. (2016). The association between polyunsaturated fatty acid consumption and the transition to psychosis in ultra-high risk individuals Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA), 108, 30-37 DOI: 10.1016/j.plefa.2016.03.010Newbury J, Arseneault L, Caspi A, Moffitt TE, Odgers CL, &am... Read more »
Pawełczyk, T., Trafalska, E., Kotlicka-Antczak, M., & Pawełczyk, A. (2016) The association between polyunsaturated fatty acid consumption and the transition to psychosis in ultra-high risk individuals. Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA), 30-37. DOI: 10.1016/j.plefa.2016.03.010
Newbury J, Arseneault L, Caspi A, Moffitt TE, Odgers CL, & Fisher HL. (2016) Why are Children in Urban Neighborhoods at Increased Risk for Psychotic Symptoms? Findings From a UK Longitudinal Cohort Study. Schizophrenia bulletin. PMID: 27153864
Not all habits are bad. Some are even necessary. It's a good thing, for example, that we can find our way home on "autopilot" or wash our hands without having to ponder every step. But inability to switch from acting habitually to acting in a deliberate way can underlie addiction and obsessive compulsive disorders.
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Christina M. Gremel,, Jessica H. Chancey,, Brady K. Atwood,, Guoxiang Luo,, Rachael Neve,, Charu Ramakrishnan,, Karl Deisseroth,, David M. Lovinger, & Rui M. Costa. (2016) Endocannabinoid Modulation of Orbitostriatal Circuits Gates Habit Formation. Neuron. info:/10.1016/j.neuron.2016.04.043
Dynamic positioning of lysosomes in the cytoplasm plays an important role in their function and is, in part, regulated by cellular nutrient status. The FLCN/FNIP complex is known to be active on the lysosome surface, where it interacts with Rag GTPases, supports the nutrient‐dependent recruitment and activation of mTORC1, and regulates the localisation of lysosome associated transcription factors (Petit et al., 2013; Tsun et al., 2013). New research from Starling et al. (2016) now shows that folliculin (FLCN) also controls the dynamic cytoplasmic position of the lysosome itself.... Read more »
Starling GP, Yip YY, Sanger A, Morton PE, Eden ER, & Dodding MP. (2016) Folliculin directs the formation of a Rab34-RILP complex to control the nutrient-dependent dynamic distribution of lysosomes. EMBO reports. PMID: 27113757
Performing the discrete mode of presentation test strongly enhances the salience of the relevant variable, perimeter, and somewhat decreases that of area. This enhancement supports appropriate solution strategies that lead to improved performance. This effect is robust and transfers to continuous mode of presentation for at least 10 days. In line with this conclusion, a student who performed the continuous test after the discrete one commented that, “It [continuous] was harder this time but I used the previous shapes, because I could do tricks with the matchsticks.”... Read more »
Babai, R., Nattiv, L., & Stavy, R. (2016) Comparison of perimeters: improving students’ performance by increasing the salience of the relevant variable. ZDM, 48(3), 367-378. DOI: 10.1007/s11858-016-0766-z
The topic prevention of brain disorders is commonly neglected. This is despite increasing evidence for evidence-based support for prevention opportunities.This issue is highlighted in a recent study out of Finland that examined prenatal nicotine metabolite levels and offspring diagnosis of schizophrenia.In this study, Solja Niemela and the Finnish research team examined all live births in Finland between 1983 and 1998.What makes this study powerful is the measurement of maternal serum cotinine levels in maternal serum during the early and mid stages of prenancy. Cotinine is a metabolite and the levels of cotinine reflect the level of nicotine consumption.The key findings from this study include the following points:Measuring cotinine levels as a continuous variable yielded an increased odds ratio for schizophrenia of 3.41 (95% CI 1.86-6.24)Mothers in the highest cotinine level group had a 38% increase in offspring schizophrenia ratesThese findings included controlling for potential confounding variables including maternal age and parental history of psychiatric disordersInterestingly a PubMed search found a second study linking maternal smoking with increased risk of offspring diagnosis of bipolar disorder (odds ratio 2.01, 95% CI 1.48-2.53).These two studies in combination support a potential non-specific effect of prenatal nicotine exposure on risk for two of the most impairing psychiatric disorders. These two studies also support aggressive smoking cessation efforts in young women before pregnancy or at the latest very early after conception.You can find more information about these two studies by clicking on the citation links below.Follow the author on Twitter WRY999Photo of pair of pin-tail ducks is from my files.Niemelä, S., Sourander, A., Surcel, H., Hinkka-Yli-Salomäki, S., McKeague, I., Cheslack-Postava, K., & Brown, A. (2016). Prenatal Nicotine Exposure and Risk of Schizophrenia Among Offspring in a National Birth Cohort American Journal of Psychiatry DOI: 10.1176/appi.ajp.2016.15060800 Talati A, Bao Y, Kaufman J, Shen L, Schaefer CA, & Brown AS (2013). Maternal smoking during pregnancy and bipolar disorder in offspring. The American journal of psychiatry, 170 (10), 1178-85 PMID: 24084820... Read more »
Niemelä, S., Sourander, A., Surcel, H., Hinkka-Yli-Salomäki, S., McKeague, I., Cheslack-Postava, K., & Brown, A. (2016) Prenatal Nicotine Exposure and Risk of Schizophrenia Among Offspring in a National Birth Cohort. American Journal of Psychiatry. DOI: 10.1176/appi.ajp.2016.15060800
Talati A, Bao Y, Kaufman J, Shen L, Schaefer CA, & Brown AS. (2013) Maternal smoking during pregnancy and bipolar disorder in offspring. The American journal of psychiatry, 170(10), 1178-85. PMID: 24084820
I know that I'm probably starting to sound like a broken record on the topic of wandering (elopement) and autism on this blog (see here and see here and see here) but I am yet again going to briefly talk about peer-reviewed research in this area simply because it's just too damned important not to.This time around the results from Catherine Rice and colleagues  are the source of my musings and the conclusion that: "wandering among children with ASD [autism spectrum disorder], regardless of intellectual disability status, is relatively common." Based on the analysis of data from The Survey of Pathways to Diagnosis and Services (SPDS) initiative, where specific questions about 'wandering and wandering prevention' are asked (see page 29) researchers reported that: "For children with special healthcare needs diagnosed with either ASD, intellectual disability, or both, wandering or becoming lost during the previous year was reported for more than 1 in 4 children." A diagnosis of ASD seemed to be a key factor in the frequency of wandering, where those with additional learning disability were the most likely to wander (37% of the sample) and figures for those without intellectual disability came in at about 32%.As per previous occasions when I've blogged about this topic, the differences (kingdoms) that might divide various groups/people when it comes to autism tend to take second place when it comes to tackling this issue and preventing (yes, preventing) wandering from turning into something rather more ominous. After all, there are a range of measures that can be employed to reduce the frequency of wandering/elopement and, if and when it does happen, reduce the probability of 'adverse outcomes' for the wanderer. First and foremost I would say, is for more people to take note of actual accounts about wandering as per those discussed by Solomon and Lawlor  for example. One can learn a lot about the circumstances around why wandering occurs and the different types of wandering (including the issue of bolting) from listening to parent and caregiver accounts. They are the experts on their own children and no doubt some of those accounts might generalise to more than just one child.Next up are the various instruments that could be used to help find wanderers in a timely fashion. I'm thinking specifically about technology such as GPS trackers and the need for science to provide some further insight into the effectiveness of such items and what needs to be done to improve their effectiveness. I appreciate that 'tracking people' might have implications for things like civil liberties but just remember that the mobile (cell) phone you're carrying might not also be bad at telling others where you are. Improving autism awareness among first responders such as police and related agencies may also help them in their efforts if and when wandering becomes an issue.Finally and bearing in mind that 'if you've met one person with autism, you've met one autistic person' (or words to that effect) is the importance of teaching things like road and water safety to those on the autism spectrum. I appreciate that the concept of 'danger' might not be something easily taught to some children and communication issues can be barriers to effective teaching. But, one should not assume that it is impossible to do , alongside the strategies for making lessons like swimming classes for example 'fun' as well as potentially lifesaving. And yes, swimming lessons can be particularly fun for many children on the autism spectrum .---------- Rice CE. et al. Reported Wandering Behavior among Children with Autism Spectrum Disorder and/or Intellectual Disability. J Pediatr. 2016 May 2. pii: S0022-3476(16)00428-5. Call NA. et al. Clinical outcomes of behavioral treatments for elopement in individuals with autism spectrum disorder and other developmental disabilities. Autism. 2016 May 12. pii: 1362361316644732. Eversole M. et al. Leisure Activity Enjoyment of Children with Autism Spectrum Disorders. J Autism Dev Disord. 2016 Jan;46(1):10-20.----------Rice, C., Zablotsky, B., Avila, R., Colpe, L., Schieve, L., Pringle, B., & Blumberg, S. (2016). Reported Wandering Behavior among Children with Autism Spectrum Disorder and/or Intellectual Disability The Journal of Pediatrics DOI: 10.1016/j.jpeds.2016.03.047... Read more »
Rice, C., Zablotsky, B., Avila, R., Colpe, L., Schieve, L., Pringle, B., & Blumberg, S. (2016) Reported Wandering Behavior among Children with Autism Spectrum Disorder and/or Intellectual Disability. The Journal of Pediatrics. DOI: 10.1016/j.jpeds.2016.03.047
I discuss how global warming may affect the reproductive success of male lions.... Read more »
West PM, & Packer C. (2002) Sexual selection, temperature, and the lion's mane. Science (New York, N.Y.), 297(5585), 1339-43. PMID: 12193785
by Piter Kehoma Boll Males and females are defined by their gametes. Males have tiny, usually mobile gametes, while females have very large gametes that usually do not move. This means that females produce less gametes, but put a lot … Continue reading →... Read more »
Córdoba-Aguilar, A., Vrech, D., Rivas, M., Nava-Bolaños, A., González-Tokman, D., & González-Soriano, E. (2014) Allometry of Male Grasping Apparatus in Odonates Does Not Suggest Physical Coercion of Females. Journal of Insect Behavior, 28(1), 15-25. DOI: 10.1007/s10905-014-9477-x
Did you know that there may be bits of your own body that you don't own? That may be owned by someone else? No?? Then you need to know more about Gene Patenting...... Read more »
Rosenfeld, J., & Mason, C. (2013) Pervasive sequence patents cover the entire human genome. Genome Medicine, 5(3), 27. DOI: 10.1186/gm431
Liddicoat J, Whitton T, & Nicol D. (2015) Are the gene-patent storm clouds dissipating? A global snapshot. Nature biotechnology, 33(4), 347-52. PMID: 25850055
AG McCluskey. (2016) Patent-ly Obvious..?. Zongo's Cancer Diaries. info:/
Like it or not: Our discipline is very much dominated by positivism and the application of the scientific method, which assumes that new knowledge can be created by developing and testing theory or, in other words, by induction or deduction. Another type of inference is abduction. Spens & Kovács (2006) present an overview of the […]... Read more »
Spens, K., & Kovács, G. (2006) A Content Analysis of Research Approaches in Logistics Research. International Journal of Physical Distribution , 36(5), 374-390. DOI: 10.1108/09600030610676259
An investigational app and online program to reduce alcohol intake is now available free to the public.This tool is an application of cognitive bias modification. A link to a study supporting cognitive bias modification is noted in the citation below. Click on the PMID link to get to the abstract.The program uses a 15 minutes per day tool for four days.The program was developed at the London School of Economics by Professor Paul Dolan.Users who sign up to use the tool will be providing data to further determine the effectiveness of the app.Read more about this tool at Science Daily HERE.A link to the program and app can be found HERE.Follow me on Twitter @WRY999 HERE.Photo of painting titled "Peasants Enjoying a Beer at Pub in Fribourg" is from Wikipedia Creative Common file. Citation: By François Louis Jaques (1877–1937) (Beurret & Bailly) [Public domain], via Wikimedia CommonsGladwin TE, Rinck M, Eberl C, Becker ES, Lindenmeyer J, & Wiers RW (2015). Mediation of cognitive bias modification for alcohol addiction via stimulus-specific alcohol avoidance association. Alcoholism, clinical and experimental research, 39 (1), 101-7 PMID: 25623410... Read more »
Gladwin TE, Rinck M, Eberl C, Becker ES, Lindenmeyer J, & Wiers RW. (2015) Mediation of cognitive bias modification for alcohol addiction via stimulus-specific alcohol avoidance association. Alcoholism, clinical and experimental research, 39(1), 101-7. PMID: 25623410
If you feel brave enough, today I will direct your reading attention to the paper by Michael Williams and colleagues  detailing the application of a particularly important genome editing technique called CRISPR-Cas9  to autism-related science.Titled: "A Retroviral CRISPR-Cas9 System for Cellular Autism-Associated Phenotype Discovery in Developing Neurons" the Williams paper probably won't win any awards for plain English but don't be fooled about just how important this paper might be in the grand era of 'we can edit genomes' and how this might translate into modelling particular types of autism or genetic issues linked to autism in mice or other animals for example.I really wish that I could say I was an expert on CRISPR-Cas9 and understood every detail included in the Williams paper but alas, I'm not and I didn't. Bearing in mind my non-expertise ('a cobbler should stick to his last') I did want to include it on this blog given the excitement in this area. Take my observations however, with a large pinch of salt...So a definition of CRISPR [clustered regularly interspaced short palindromic repeats] -Cas9 - well, I don't want to reinvent the wheel so I'll use that offered in reference  with full credit given to the writer (Steph Yin): "Here’s how CRISPR/Cas works in bacteria: When bacteria encounter an invading source of DNA, such as from a virus, they can copy and incorporate segments of the foreign DNA into their genome as “spacers” between the short DNA repeats in CRISPR. These spacers enhance the bacteria’s immune response by providing a template for RNA molecules to quickly identify and target the same DNA sequence in the event of future viral infections. If the RNA molecules recognize an incoming sequence of foreign DNA, they guide the CRISPR complex to that sequence. There, the bacteria’s Cas proteins, which are specialized for cutting DNA, splice and disable the invading gene." The application of this process outside of just bacteria was subsequently recognised and a 'gene editing tool' was eventually born whereby a CRISPR-Cas9 system could replace any gene sequence.Clear as mud right?Well, Williams et al add to a small but emerging peer-reviewed research base at the time of writing suggesting that CRISPR-Cas9 might provide some important insights into at least 'some' autism. Their particular idea was to "mimic nonsense PTEN mutations from autism patients in developing mouse neurons" on the back of some previous research suggesting that various genetic issues with PTEN might be present in some autism . Nonsense mutation by the way, normally ends in 'nonfunctional proteins' based on the knowledge that [some] genes provide the template to make proteins.To achieve such mutations in PTEN authors used "retroviral implementation of the CRISPR-Cas9 system" where engineered retroviruses were purposed to deliver something mimicking a genetic mutation previously noted in cases of autism that were then injected into "the hippocampus of postnatal day 7 (P7) mice." Researchers then monitored the retrovirus infected cells to see what they looked like in terms of carrying the mutation and hence showing loss of PTEN function or not. They noted that there was a degree of 'hit-and-miss' based on their approach but were "able to clearly discern the established hypertrophic phenotype due to loss of Pten function across the cell population on average."Not content with such molecular engineering, authors also turned their attention to designing viruses "to target a gene that has recently been associated with autism, KATNAL2." KATNAL2 has been described by other authors as a 'genuine' autism risk factor  (er, right...) and on that basis researchers designed a retrovirus carrying a mutation designed to disrupt expression of the gene. After some preliminary work to test out how successful their retrovirus delivered mutation was in the test tube, they injected it and/or a control retrovirus into the brain of another set of mice. They found some interesting changes in the experimental retrovirus-infected brains pertinent to "decreased dendritic arborization of developing neurons." In layman's terms this equates as evidence of "disruption of normal neuronal development" that "may lead to synaptic circuit dysfunction underlying the autism phenotype."As per my earlier 'pinch of salt' sentiments I am not offering any authoritative opinion about the Williams paper and the techniques included. My interpretation is just that; interested readers are advised to do a little more reading around this subject before quoting my text as 'truth'. What I do hope that I've got across is the message that CRISPR-Cas9 and the delivery of engineered genetic mutations via something like a retrovirus is already here and will no doubt be impacting on autism research in times to come. In an era where 'the autism gene' has been replaced by a more general model of many different genes potentially producing many different autisms (see here), one can perhaps see how focusing in on specific genes linked to 'some' autism might be ripe for this kind of analysis (see here). I say all that recognising that whilst many would love to be able to say that autism is solely a genetic condition, the role of non-genetic factors variably affecting risk is not to be forgotten (see here).We will see what else emerges in the peer-reviewed domain in this brave new world...---------- Williams MR. et al. A Retroviral CRISPR-Cas9 System for Cellular Autism-Associated Phenotype Discovery in Developing Neurons. Sci Rep. 2016 May 10;6:25611. Yin S. What Is CRISPR/Cas9 and Why Is It Suddenly Everywhere? Motherboard. 2015. April 30. Neale BM. et al. Patterns and rates of exonic de novo mutations in autism spectrum disorders. Nature. 2012 Apr 4;485(7397):242-5.----------Williams MR, Fricano-Kugler CJ, Getz SA, Skelton PD, Lee J, Rizzuto CP, Geller JS, Li M, & Luikart BW (2016). A Retroviral CRISPR-Cas9 System for Cellular Autism-Associated Phenotype Discovery in Developing Neurons. Scientific reports, 6 PMID: 27161796... Read more »
Williams MR, Fricano-Kugler CJ, Getz SA, Skelton PD, Lee J, Rizzuto CP, Geller JS, Li M, & Luikart BW. (2016) A Retroviral CRISPR-Cas9 System for Cellular Autism-Associated Phenotype Discovery in Developing Neurons. Scientific reports, 25611. PMID: 27161796
Feelings of shame and humiliation bother obese air passengers more than tight seat belts and tiny seats, according to a study published by Ben-Gurion University of the Negev (BGU) researchers. Participants interviewed for the study recounted the typical challenges they encounter while boarding, in-flight and deplaning.
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Yaniv Poria, & Jeremy Beal. (2016) An Exploratory Study about Obese People’s Flight Experience . Journal of travel research. info:/10.1177/0047287516643416
The most comprehensive index of open access journals, the Directory of Open Access Journals (DOAJ), reviewed its inclusion criteria, in view of allegations of the presence of predatory journals. This restructuring will lead to more than 3,000 journals to be removed from the database. DOAJ, besides advocating Open Access, established, in collaboration with COPE, OASPA and WAME, a code of principles and good practices in scientific publishing. … Read More →... Read more »
There are many risk factors for Alzheimer's Disease (AD) including history of head trauma and family history of AD.The strongest risk factor is advanced age. Yearly risk for AD is about 1% per year in 70 year old populations jumping to around 7% in 90 year old groups.Now a recent study is shedding some light on a new risk for AD in men. This risk appears to be related to a chromosome Y phenomenon known to be associated with aging.Elderly men show a tendency to lose the Y chromosome from a small percentage of cells over time. This phenomenon is known as loss of Y or LOY.The percentage of blood cells with LOY can be determined. A study recently published in Journal of Human Genetics (see citation below) found significant support for higher percentage of LOY being linked to AD risk.Here are the key findings:In a sample of 3218 elderly men 17% showed evidence of LOY chromosome mosaicismLOY percentage rates were strongly positively correlated with older ageMen with AD had higher rates of LOY than age-matched men without AD (adjusted odds ratio=2.80)Two prospective studies found higher rates of incident AD in men with LOY (adjusted odds ratio=6.80)These findings are not simply minor as the effect of LOY on risk appears similar in magnitude to the strongest genetic risk factor for AD, APOE gene status.LOY has also been linked to a higher risk of cancer, so it appears to be a non-specific risk factor.The authors of this study note;"Regardless of the underlying mechanism(s) for the increased risk of AD and cancer in men with LOY in blood, our and other's published results reinforce a role of factors on chromosome Y in various, still poorly explored biological processes, other than sex determination and sperm production."LOY is not yet a common test in clinical practice. However, I think we will be hearing much more on this association with potential for screening and intervention studies.Access the free full-text manuscript by clicking on the DOI link in the citation below.Follow me on Twitter WRY999Photo of eastern screech owl is from my photo files.d sperm production.Dumanski JP et al (2016). Mosiac loss of chromosome Y in blood is associated with Alzheimer's disease American Journal of Human Genetics : 10.1016/j.ajhg.2016.05.014... Read more »
Dumanski JP et al. (2016) Mosiac loss of chromosome Y in blood is associated with Alzheimer's disease. American Journal of Human Genetics. info:/10.1016/j.ajhg.2016.05.014
The fight against aging Ever since the ancient Sumerians, men has sought eternal life. We still do. Anti-aging science has become quite an industry. As we dive deeper and deeper into our biological foundations, we’re learning more and more about how and why we age. A lot of mysteries remain, but there’s still talk about […]... Read more »
There are many tools at NCBI, with a huge range of functions. Literature, sequence data, variations, protein structure, chemicals and bioassays, and more. It’s hard to keep track of what’s available. Their video tutorials are helping me to be aware of new tools, and new features within existing tools. For this week’s Tip of the […]... Read more »
Kapustin, Y., Souvorov, A., Tatusova, T., & Lipman, D. (2008) Splign: algorithms for computing spliced alignments with identification of paralogs. Biology Direct, 3(1), 20. DOI: 10.1186/1745-6150-3-20
NCBI staff. (2016) Database resources of the National Center for Biotechnology Information. Nucleic Acids Research, 44(D1). DOI: 10.1093/nar/gkv1290
Just like some people have a tendency to go overboard, so do some immune systems. Here’s all the ways that your immune system can get it wrong and leave you with allergies – and how some allergies can save your life.... Read more »
Calboli FC, Cox DG, Buring JE, Gaziano JM, Ma J, Stampfer M, Willett WC, Tworoger SS, Hunter DJ, Camargo CA Jr, Michaud DS. (2011) Prediagnostic plasma IgE levels and risk of adult glioma in four prospective cohort studies. J Natl Cancer Inst. . DOI: 10.1093/jnci/djr361
Joseph A Jackson, Ida M Friberg, Luke Bolch, Ann Lowe, Catriona Ralli, Philip D Harris, Jerzy M Behnke, Janette E Bradley. (2009) Immunomodulatory parasites and toll-like receptor-mediated tumour necrosis factor alpha responsiveness in wild mammals. BMC Biology. DOI: 10.1186/1741-7007-7-16
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