For 60 years, the standard procedure for heart surgery was to open the chest. Then, bypass surgery (replacing clogged coronary arteries), transplants, and other procedures could be performed. While open—heart surgery was revolutionary enough when it was introduced in the 1960s, now a new revolution is taking place—heart surgery without cutting open the chest. Or at least not as much... Read more »
Iribarne, A., Easterwood, R., Chan, E., Yang, J., Soni, L., Russo, M., Smith, C., & Argenziano, M. (2011) The golden age of minimally invasive cardiothoracic surgery: current and future perspectives. Future Cardiology, 7(3), 333-346. DOI: 10.2217/fca.11.23
I'm very conscious of the fact that I tend to talk quite a lot about biological research on this blog and its potential implications for people on the autism spectrum and beyond. To some, this can seem a little one-sided in terms of how autism is viewed and indeed at the expense of a large proportion of people on the autism spectrum who are not necessarily looking to understand how cytokines or dietary intervention for example, might impact on their signs, symptoms or everyday quality of life.You're hired @ Wikipedia Indeed, accepting that the autism spectrum is wide and heterogeneous, for some on the autism spectrum there are more pressing issues which impact on their daily life such as the impact of comorbidities including anxiety and/or obsessions, and under certain circumstances, how these features can truly disable a person.In this post therefore I want to try and address some of the issues looking at a key part of many people's lives: employment and unemployment, and some of the variables around employment for adults with an autism spectrum condition which might help or hinder their efforts to enter the workplace with a particular focus on job-seeking.I was brought to this topic by the paper from Dorothy Strickland and colleagues*, and their study looking at the potential usefulness of the JobTIPS employment program (free by the way) in helping a group of young adults with autism getting through the dreaded job interview.TransitionWhere to start, where to start? Well, in amongst the various issues that can impact the life of a person with autism, particularly those diagnosed with Asperger syndrome or the so-called 'high-functioning' autism, the transition from child to adult must rank as one of the more stressful periods. The jump from the very organised and very arranged world of school / home schooling and further education into the unknown jungle of adult life and the jobs market is riddled with pressures, not just for the individual but their family and carers too. And let's face it, with the current economic climate as it is, that jobs jungle is very much living up to its name, with many people often 'fighting it' out for each post.The job specConsider how then a potential employer tries to find that ideal candidate and what qualities they generally look for in a person. Obviously they want someone who is qualified to do the job, someone who is reliable and someone who is enthusiastic. OK, no real surprises there. But then you get phrases like a 'good communicator', a 'team player' and the like also appearing in the job specification and suddenly the job spec is no longer about having certain skills for a job. I think you can perhaps see how daunting these additional specs might be for someone who is perhaps not a great talker (or indeed likes to dominate a conversation with their own talking) or who might not generally be at their most comfortable in that team player role.The application formThen comes the next hurdle: the application form. What is your name? OK, that's easy enough, as is the other information which is explicitly asked for with closed questions. Your educational achievements and your contact details, no real issues there too. But then come the open-ended questions. What do you like to do in your spare-time? What are your biggest achievements? Why do you think you are the best candidate for this job? How one answers such questions is very much going to depend on how one is able to translate these questions and in some cases how literally one understands such questions within their own experiences and interests.The job interviewAssuming these hurdles are past, the final stage is the job interview. Y'know all those tips that seem to percolate through the web on 'how to get that dream job'. Be confident but not overly-confident. Eye contact and the occasional smile or other gesture to lighten up the whole experience. A bit of chit-chat on certain topics (as long as you stay on topic and answer the questions). In short: go in there and sell yourself.All well and good if you are so inclined to such skills. But readers can perhaps see how for those who might be more than a little bit anxious about the whole process - in particular the 'not knowing' about the process - for those who perhaps don't read social cues as others might, or find that using and maintaining appropriate eye contact to be somewhat distressing, might be placed at some disadvantage. And then there are those seemingly obscure questions which seem to drop into interviews to either make the interviewee think on their feet or have some hidden psychological meaning....The point I want to get across in this post is that one can perhaps see how the job interview process from start to finish is not exactly 'friendly' to many people on the autism spectrum and how some very subtle changes and amendments to elements of the process might level the playing field. I'm not necessarily supporting a call to introduce any positive discrimination or sheltered employment initiatives because such policies can create their own issues. That being said, for potential employers to look at their recruitment policies and think about how many very talented people might be slipping through their admissions net for the sake of a few details, might not be a huge undertaking bearing in mind that work also brings its own stresses.To finish, a few dos and don'ts for any job interview and some handy hints for any would-be employer interviewing someone with an autism spectrum condition for a job courtesy of the NAS.Oh, and the eagle-eyed reader might have spotted that the picture accompanying this post is the old (very old) Amstrad CPS 464. So posted because of the founder of Amstrad and his quite well-known catch-phrase 'You're fired/hired'.-----------* Strickland DC. et al. JobTIPS: A transition to employment program for individuals with autism spectrum disorders. J Autism Dev Disord. March 2013.---------- Strickland DC, Coles CD, & Southern LB (2013). JobTIPS: A Transition to Employment Program for Individuals with Autism Spectrum Disorders. Journal of autism and developmental disorders PMID: 23494559... Read more »
Strickland DC, Coles CD, & Southern LB. (2013) JobTIPS: A Transition to Employment Program for Individuals with Autism Spectrum Disorders. Journal of autism and developmental disorders. PMID: 23494559
A blog post summarising some of the findings in a major molecular epidemiological study of Blastocystis in non-human primates, including apes, Old and New World monkeys, and prosimians.... Read more »
Yildirim S, Yeoman CJ, Sipos M, Torralba M, Wilson BA, Goldberg TL, Stumpf RM, Leigh SR, White BA, & Nelson KE. (2010) Characterization of the fecal microbiome from non-human wild primates reveals species specific microbial communities. PloS one, 5(11). PMID: 21103066
ALFELLANI, M., JACOB, A., PEREA, N., KRECEK, R., TANER-MULLA, D., VERWEIJ, J., LEVECKE, B., TANNICH, E., CLARK, C., & STENSVOLD, C. (2013) Diversity and distribution of Blastocystis sp. subtypes in non-human primates. Parasitology, 1-6. DOI: 10.1017/S0031182013000255
Stensvold CR, Arendrup MC, Nielsen HV, Bada A, & Thorsen S. (2008) Symptomatic infection with Blastocystis sp. subtype 8 successfully treated with trimethoprim-sulfamethoxazole. Annals of tropical medicine and parasitology, 102(3), 271-4. PMID: 18348782
Stensvold CR, Alfellani M, & Clark CG. (2012) Levels of genetic diversity vary dramatically between Blastocystis subtypes. Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases, 12(2), 263-73. PMID: 22116021
CrossFit Diet: High Tomato intake help keep you from getting down, blue or depressed. Which a lot of us might be feeling now that the CrossFit Open is over. AThe post CrossFit Diet Info: Eat your vegetables or you’ll get depressed. appeared first on WODMasters Stiff Competition.... Read more »
Niu K, Guo H, Kakizaki M, Cui Y, Ohmori-Matsuda K, Guan L, Hozawa A, Kuriyama S, Tsuboya T, Ohrui T.... (2013) A tomato-rich diet is related to depressive symptoms among an elderly population aged 70 years and over: a population-based, cross-sectional analysis. Journal of affective disorders, 144(1-2), 165-70. PMID: 22840609
There have been a number of heated discussions about genetic privacy recently. Lately the discussion of the Henrietta Lacks (HeLa) genome paper erupted into wide-ranging awareness of some of the issues and complexities around genome data and family relationships. The paper by Yaniv Erlich’s team about re-identification of study participants using genealogy site details also [...]... Read more »
Presidential Commission for the Study of Bioethical Issues. (2012) Privacy and Progress in Whole Genome Sequencing. www.bioethics.gov. info:other/
Heavy tokers may be at higher risk, but alcohol is the hidden confounder.
Young people don’t suffer from strokes, as a rule. And when they do, at least half the time there is no obvious cardiovascular explanation. So it’s not surprising that drugs are often invoked as the culprit.
A New Zealand study earlier this year once again raised the specter of a possible link between stroke and marijuana smoking. As reported by Maia Szalavitz at Time Healthland, the confounding issue, as is typical of such studies, is the coexisting use of other drugs, like alcohol and cigarettes. As Szalavitz writes:
The stroke study, which incorporated preliminary data, is the first trial of its kind to study a possible connection between marijuana use and stroke. It included 160 patients aged 18 to 55 who had suffered a stroke connected to a blood clot in the brain, and who agreed to have their urine tested for marijuana within 72 hours of the stroke. These results were compared to those from 160 controls who had not had a stroke but came to the hospital for other reasons. They were matched on age, gender and ethnic background, all of which can also affect the risk for this type of stroke. About 16% of the stroke patients showed traces of marijuana in their urine, compared to 8% of those in the control group, suggesting a doubling of the risk of stroke.
However, because of nicotine and other confounding variables, that study was considered inconclusive. In an earlier study published in Stroke, the journal of the American Heart Association, Valerie Wolff and colleagues from the University of Strasbourg in France searched the medical literature and found 59 cases of stroke in which cannabis could be considered a cardiovascular risk factor. The investigators used only cases that had been confirmed by neuroimaging. The researchers focused on cases where a stroke had occurred while smoking marijuana, or within a half hour after the last joint or bong hit.
But proving a cause and effect relationship is tricky. Assuming, for now, that all of the strokes in question were not caused or compounded by alcohol or drugs other than marijuana, the French scientists postulated several mechanisms that could conceivably account for a cannabis-related ischemic stroke (a stroke caused by obstruction of a blood vessel). These include orthostatic hypotension, altered cerebral vasomotor function, major swings in blood pressure, and cardiac arrhythmias. However, the only solid commonality in cannabis-related strokes was that the users were more likely to be heavy smokers.
In the 50 strokes the researchers were able to confirm by cerebral imaging, the patterns in some patients were similar to those observed in a syndrome called reversible cerebral vasoconstriction syndrome (RCVS). RCVS is marked by severe headaches, strokes, and brain edema, but symptoms typically resolve in a few months. “Reversibility of the vasoconstriction within 12 weeks is a key point of this syndrome,” the authors write. “The long duration of stenosis [blockage] argues in favor of a drug-induced immunoallergic vasculitis rather than vasospasm. Our point of view is that this disorder may be considered as a variant of RCVS,” rather than as a garden-variety ischemic stroke triggered by excessive use of cannabis.
According to the French study, “The most frequently presented characteristics of cannabis users who experienced a stroke are young male chronic tobacco and cannabis abusers who have had an unusual high consumption of cannabis and alcohol before stroke.” The most convincing mechanism to explain ischemic strokes in young people, the researchers say, is “reversible cerebral angiopathy involving several arteries, associated with cannabis consumption in association with tobacco and alcohol use.”
And there you have it. Smoke weed, and you appear to have a slight risk of suffering stroke, which, under age 50, is an extremely uncommon medical event. Add tobacco, and the stroke risk goes up. Add alcohol, and the stroke risk ratchets even higher. By itself, marijuana appears to be a minor factor in strokes—but it appears likely that pot is indeed the culprit at least some of the time.
“Cannabis-related stroke is not a myth,” the scientists conclude, “and a likely mechanism of stroke in most cannabis users is the presence of reversible multifocal intracranial stenosis (MIS) induced by this drug. The reality of the relationship between cannabis and stroke is, however, complex, because other confounding factors have to be considered (ie, lifestyle and genetic factors).”
Wolff V., Armspach J.P., Lauer V., Rouyer O., Bataillard M., Marescaux C. & Geny B. (2013). Cannabis-related Stroke: Myth or Reality?, Stroke, 44 (2) 558-563. DOI: 10.1161/STROKEAHA.112.671347
Graphics Credit: http://www.strokegenomics.org/
... Read more »
Remember this study from a week ago, where researchers showed L-acetyl carnitine rapidly alleviating depression symptoms by changing DNA expression? Well, a new study in Nature Medicine now identified a compound in red meat that can be metabolized by our gut microbiota into TMAO, which promotes atherosceleosis. And the culprit? L-carnitine, the parent compound of [...]... Read more »
Koeth, R., Wang, Z., Levison, B., Buffa, J., Org, E., Sheehy, B., Britt, E., Fu, X., Wu, Y., Li, L.... (2013) Intestinal microbiota metabolism of l-carnitine, a nutrient in red meat, promotes atherosclerosis. Nature Medicine. DOI: 10.1038/nm.3145
There are some key 'go-to' peer-reviewed texts which I've found to be useful when talking about the various conditions on the autism spectrum. On the topic of Asperger syndrome, I've always tended to come back to the paper by Tom Berney* (open-access) charting the progression of the condition through childhood into adulthood.The whisper of the Muse @ Wikipedia Despite being published nearly 10 years ago, the paper by Dr Berney weathers well and covers many of the discussions which have come to the forefront in recent years including education and employment prospects, the potential for overlap with the schizophrenia spectrum and the difficult issue of offending behaviour.Indeed the first place I went looking after reading the paper by Conor Davidson and colleagues** highlighting the prevalence of Asperger syndrome (AS) in cases of first-episode psychosis (3.6%), was the Berney paper to see if this was something new, a rehash of what is already known about or just a chance event. Turns out there was a pearl of wisdom in there as per his observations on 'mistaking Asperger syndrome for psychosis' and in particular "high arousal in a developmental disorder can produce an acute and transient psychotic state with hallucinations and thought disorder".I'm sorry that I can't post a link to the full-text of Dr Davidson's paper but take my word for it that it is an interesting piece of research, well thought out and well executed. Without wishing to plagiarise the work, there is an interesting case study nestled among the data, describing the experiences of one participant and his lifelong features of AS which were seemingly not picked up by any agency. In particular the description demonstrates how following the transition from home environment to University, the new social demands contributed to him "eschewing all human contact" and after a period of issues with eating and sleeping he developed grandiose delusions with a theme of absolute control over others: "I'm studying neuroscience to take over people's minds... take over the world... become immortal and invincible". Apparently Tony Attwood has previously described this 'God mode'.OK, let's back up here a little and put this in context. I've said it many times before on this blog, how a diagnosis within the autism spectrum is seemingly protective of nothing when it comes to comorbidity. That people diagnosed and living with an autism spectrum condition might also be more prone to various other psychiatric comorbidity particularly into young adulthood is no big secret (see this paper by Lugnegård and colleagues*** for example) and has been raised before on this blog.Yes, one could look to that recent Lancet study**** as being evidence that there may be a genetic 'fragility' towards common ground between autism and other conditions but let's not get too ahead of ourselves when it comes to all things genetic. The important caveats being that such psychiatric comorbidity is by no means a universal phenomenon to everyone with autism, and realising the potentially important effects that a person's environment for example, has on the presentation or protection against said comorbidity (social circles and support, living conditions, employment, finances, etc.). Oh and the possible involvement of a few more biological factors too...Still I find myself intrigued by the Davidson findings and their suggestions about clinicians being "alert to the possibility of Asperger syndrome when assessing patients" presenting with psychosis. Not least because of the implications for the appropriate detection and assessment of Asperger syndrome; only in this study becoming apparent to health care professionals when the individual was presenting with first-episode psychosis.Questions, questions, questions: why were these young adults not initially 'picked-up' for an autism spectrum conditions when younger, as per the Berney statement, was Asperger syndrome to 'blame' for their psychosis presentation, and what are the longer-term implications of Asperger syndrome for example related to other future episodes of psychosis and their management?Added into the mix too are papers like this one from James MacCabe and colleagues***** which suggested that a decline in cognitive performance and verbal ability during the adolescent years might translate into an increased risk for psychosis in adulthood. If so, could this be a potential way of differentiating Asperger syndrome + psychosis from psychosis as a result of Asperger syndrome and that 'high arousal' quoted by Berney? Indeed on the back of the paper by Sönmez and colleagues****** (open-access) is there also a tie-up between first-episode psychosis, depression and Asperger syndrome too?I haven't got any specific answers to these questions by the way, aside from reaffirming my line about a diagnosis of an autism spectrum condition being seemingly protective of nothing when it comes to somatic or psychiatric comorbidity. Oh and the need for appropriate services and support to identify and if possible, mitigate such comorbidity as and when it does present.----------* Berney TP. Asperger syndrome from childhood into adulthood. Adv Psychiatr Treat. 2004; 10: 341-351.** Davidson C. et al. Prevalence of Asperger syndrome among patients of an Early Intervention in Psychosis team. Early Interv Psychiatry. March 2013.*** Lugnegård T. et al. Psychiatric comorbidity in young adults with a clinical diagnosis of Asperger syndrome. Res Dev Disabil. 2011; 32: 1910-1917.**** Cross-Disorder Group of the Psychiatric Genomics Consortium. Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis. The Lancet. February 2013.***** MacCabe JH. et al. Decline in cognitive performance between ages 13 and 18 years and the risk for psychosis in adulthood. JAMA Psychiatry. 2013; 70: 261-270.****** Sönmez N. et al. Depressive symptoms in first episode psychosis: a one-year follow-up study. BMC Psychiatry 2013; 13: 106.----------Davidson C, Greenwood N, Stansfield A, & Wright S (2013). Prevalence of Asperger syndrome among patients of an Early Intervention in Psychosis team. Early intervention in psychiatry PMID: 23472601... Read more »
Davidson C, Greenwood N, Stansfield A, & Wright S. (2013) Prevalence of Asperger syndrome among patients of an Early Intervention in Psychosis team. Early intervention in psychiatry. PMID: 23472601
You can probably guess that organized people are more likely to eat healthy and have a low BMI score. But did you also know that people who are less open to experiences more often like sweets? These findings, published in the new Health Psychology, may sound pretty random, which some of them may actually be, but they’re interesting food for thought.... Read more »
Mõttus, R., McNeill, G., Jia, X., Craig, L., Starr, J., & Deary, I. (2013) The associations between personality, diet and body mass index in older people. Health Psychology, 32(4), 353-360. DOI: 10.1037/a0025537
by ebender in Daily Observations
April marks a one-year milestone for APS’s newest journal Clinical Psychological Science! CPS provides a venue for cutting-edge research across a wide range of conceptual views, approaches, and topics. Since The post A Milestone for CPS appeared first on Association for Psychological Science.... Read more »
Monshouwer, K., ten Have, M., van Poppel, M., Kemper, H., & Vollebergh, W. (2012) Possible Mechanisms Explaining the Association Between Physical Activity and Mental Health: Findings From the 2001 Dutch Health Behaviour in School-Aged Children Survey. Clinical Psychological Science, 1(1), 67-74. DOI: 10.1177/2167702612450485
When it comes to knowing whether eating too much salt is a bad thing, there is a surprising lack of “verified-by-science” information available*. A certain level of salt, or sodium chloride, is a biological necessity that keeps muscles pumping and … Continue reading →... Read more »
Kleinewietfeld M, Manzel A, Titze J, Kvakan H, Yosef N, Linker RA, Muller DN, & Hafler DA. (2013) Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. Nature. PMID: 23467095
ETH researchers could show that exhaled human breath contains a characteristic molecular “fingerprint”. The scientists want to use this finding to diagnose diseases based on the chemical analysis of patient’s exhaled breath, using highly sensitive and precise instrumental methods.... Read more »
Fabio Bergamin. (2013) A fingerprint of exhaled breath. ETH Life. info:/
Viewers here in the UK might remember the catchphrase of one Michael Barrymore on the show 'Strike It Lucky': "What is a hotspot not? A good spot". It is with a rather different kind of hotspot in mind, that I'm posting about today: genomic hotspots and autism with a specific focus on copy number variants.An intriguing paper by Santhosh Girirajan and colleagues* (open-access) popped up on my Twitter radar recently discussing copy number variant (CNV) load in relation to autism spectrum disorders. Whilst only being an amateur enthusiast when it comes to all things genes and genomic, I can't offer an expert opinion on what CNVs are, just that fairly similar to single-nucleotide polymorphisms (SNPs), we're talking physical alterations to the genome and in particular gains/losses to segments of DNA (I think!)A hotspot indeed... @ Wikipedia I'll start by saying that this is not the first time that CNVs have cropped up on this blog either with autism in mind (see here) or with other conditions such as ADHD (see here) and intellectual disability (ID) in mind (see here).Indeed readers who looked at that ID link will see that we are talking about another paper from Girirajan following the previous suggestion that ID might be particularly prone to a high CNV load. Keep that in mind for now.Thankfully the latest paper has been very nicely covered by a ScienceDaily entry (see here with a sigh of relief) so as to patch over my considerable non-expertise in this area. Without plagiarising the paper or SD entry, the general gist of the work was to initially look at CNV data from over 500 people with autism (n=274) or asymptomatic controls (n=242) derived from the CHARGE initiative (see here), to ascertain exactly what the CNV load was and how it might link into some of the signs and symptoms of autism. There was also a further testing group to confirm "the increased duplication load" based on a further cohort of autism and control cases but I'm not going to bore you with all the details.If I'm reading this right, there were some interesting findings to take from this study:Children with autism "exhibited a significantly elevated copy number load, represented principally as an increase in duplicated base pairs found in large CNVs". Importantly, this copy number load seemed to include quite a bit of de novo, so not passed from parents to offspring.Duplication over deletion seemed to be the important variable for autism cases, which as the authors note "is associated with genomic variants with more modest functional impact". As per that previous CNV work with ID in mind, I think the authors seemed to be suggesting a sort of sliding scale of phenotypes based on CNV profiles: ID at the more severe end of the spectrum (with more deletions also), autism somewhere in the middle and dyslexia at the less severe end of the spectrum in terms of functioning. I could be wrong and I could be over-simplifying the whole thing so accept my apologies if so.Copy number load in autism cases also seemed to show some relationship with certain aspects of behaviour. Significant negative correlations for example, were observed between CNV load and VABS scores in core areas of communication and socialisation. That being said, the correlations were not exactly all that great (p=0.048 and p=0.022 respectively) and should be compared with other gold-standard schedules such as the ADOS that did not turn up anything significant. The notion of genomic 'hotspots' is also raised as a consequence of the results, suggesting that parts of the autistic genome already under the spotlight might be more susceptible to such CNVs. Those words-of-the-hour DNA methylation get a mention alongside the folate story (see here). Personally and with my non-expertise caveat in full working order, I'm also wondering about those archived portions of viruses called HERVs - human endogenous retroviruses - (see this post and this post) which dot the genome and whether they might be contributory in any way, shape or form to any genomic instability in target areas.Putting aside the complexity of the genome when it comes to autism and the suggestion that we might want to be rethinking how we view the condition** (I've a post coming up on this paper fairly soon), there are some interesting themes emerging from the Girirajan paper. That for example CNV load and the type of CNV (duplication or deletion) might roughly fit into phenotypic differences between inter-related conditions including autism and ID is definitely something worth pursuing in future work. That also such CNVs might tie into genomic hotspot areas is also an important point particularly when it comes to things like systems biology. Lest we also forget the potential importance of any genomic instability and how, with the DNA methylation point in mind, this *might* be attenuated via changes to the environment (remember SAMe)?To close Chuck Berry and a song about Johnny B Goode and his guitar-playing skills.----------* Girirajan S. et al. Global increases in both common and rare copy number load associated with autism. Hum. Mol. Genet. March 2013.** Moreno-De-Luca A. et al. Developmental brain dysfunction: revival and expansion of old concepts based on new genetic evidence. The Lancet Neurology. 2013; 12: 406-414.----------Girirajan S, Johnson RL, Tassone F, Balciuniene J, Katiyar N, Fox K, Baker C, Srikanth A, Yeoh KH, Khoo SJ, Nauth TB, Hansen R, Ritchie M, Hertz-Picciotto I, Eichler EE, Pessah IN, & Selleck SB (2013). Global increases in both common and rare copy number load associated with autism. ... Read more »
Girirajan S, Johnson RL, Tassone F, Balciuniene J, Katiyar N, Fox K, Baker C, Srikanth A, Yeoh KH, Khoo SJ.... (2013) Global increases in both common and rare copy number load associated with autism. Human molecular genetics. PMID: 23535821
Alzheimer’s disease (AD) is the neurodegenerative disorder that affects the brain leading to dementia. It usually occurs late in life.
Reason behind the Alzheimer’s disease:
Researchers found senile plaques and components of the plaques such as amyloid beta peptide (Abeta), which is a proteolytic fragment of the amyloid precursor protein, and neurofibrillary tangles in the brain lesions as the basic diagnosis of the AD.
Plaques found in the brain are found to be the cause of the damage to the cholinergic neurons found in the basal forebrain of the AD patients.
Drugs of choice for Alzheimer’s disease:
Among the drugs of choice for AD are donepezil HCl and tacrine, which are cholinesterase inhibitors, rivastigmine and galantamine, which are inhibitors of the breakdown of acetylcholine and memantine HCl, which is the glutamate regulator. Even the drugs of choice come with the side effects such as dizziness, headache, nausea, vomiting and insomnia.
Nutraceuticals for Alzheimer’s disease:
Recently researchers have found that many types of spices, fruits, medicinal plants and vegetables could have potential anti-oxidant activity and could help against AD.
Curcumin, yellow curry spice, has anti-oxidant and anti-inflammatory properties and could help against neurotoxic and genotoxic agents. Technically speaking, it inhibits NF-κB leading to prevention of Abeta-induced cell death in a human neuroblastoma cell line that has been considered as the therapeutic strategy for Alzheimer’s disease. It also inhibits fibril and oligomer formation, inhibit Egr-1, Abeta-induced cell death, and activation of transcription factors that is further strengthening the role of curcumin in AD treatment.
Piperine, an active alkaloid in Piper nigrum, has also shown efficacy against AD. Researchers found that the compound improved the memory impairment much in the rat model. It also improved neurodegenration in the hippocampus.
Aged garlic extract (AGE) has also showed antiamyloidogenic properties. Technically speaking, AGE suppressed the development of reactive oxygen species (ROS) that are found to be involved in the apoptotic mechanism of Abeta-mediated neurotoxicity.
(All of these compounds from 4 to 9 are found to protect the neuronal cells from Abeta-induced neurotoxicity)
(These compounds in 10 and 11 act through the inhibition of acetylcholinesterase)
Kannappan, R., Gupta, S., Kim, J., Reuter, S., & Aggarwal, B. (2011). Neuroprotection by Spice-Derived Nutraceuticals: You Are What You Eat! Molecular Neurobiology, 44 (2), 142-159 DOI: 10.1007/s12035-011-8168-2... Read more »
Kannappan, R., Gupta, S., Kim, J., Reuter, S., & Aggarwal, B. (2011) Neuroprotection by Spice-Derived Nutraceuticals: You Are What You Eat!. Molecular Neurobiology, 44(2), 142-159. DOI: 10.1007/s12035-011-8168-2
We recently published a letter in Scandinavian Journal of Gastroenterology on prevalence data on Blastocystis and Dientamoeba fragilis in patients with inflammatory bowel disease (IBD) and controls, - here's a small summary.... Read more »
Petersen AM, Stensvold CR, Mirsepasi H, Engberg J, Friis-Møller A, Porsbo LJ, Hammerum AM, Nordgaard-Lassen I, Nielsen HV, & Krogfelt KA. (2013) Active ulcerative colitis associated with low prevalence of Blastocystis and Dientamoeba fragilis infection. Scandinavian journal of gastroenterology. PMID: 23528075
Another new publication that isn’t available in full unless one is independently wealthy, but here’s the abstract. In short, 208 living kidney donors were compared with 198 two-kidneyed controls, both pre-donation and six-months post-donation. Compared with controls, donors had 28% lower glomerular filtration rates [GFR aka kidney function] at 6 months, - associated … Continue reading »... Read more »
Kasiske BL, Anderson-Haag T, Ibrahim HN, Pesavento TE, Weir MR, Nogueira JM, Cosio FG, Kraus ES, Rabb HH, Kalil RS.... (2013) A Prospective Controlled Study of Kidney Donors: Baseline and 6-Month Follow-up. American journal of kidney diseases : the official journal of the National Kidney Foundation. PMID: 23523239
A short note on the history of antidepressant research: From MAOIs/SSRIs to ketamine and BDNF Traditional antidepressants, like Prozac, don’t work too well. Back in the 50s, researchers thought that depression was caused by a depletion of a group of neurotransmitters in the brain known chemically as the monoamines (i.e. serotonin, noradrenaline, dopamine). Hence, the [...]... Read more »
Nasca C, Xenos D, Barone Y, Caruso A, Scaccianoce S, Matrisciano F, Battaglia G, Mathé AA, Pittaluga A, Lionetto L.... (2013) L-acetylcarnitine causes rapid antidepressant effects through the epigenetic induction of mGlu2 receptors. Proceedings of the National Academy of Sciences of the United States of America, 110(12), 4804-9. PMID: 23382250
Researchers have found that vitamin-P could help us in the treatment of damaged motor neurons. It can help us in potentiating the new therapeutic strategies for diseases such as Amyotrophic Lateral Sclerosis (ALS).
Molecular and Cellular Neuroscience
Vitamin P is also called as 7,8-Dihydroxyflavone. Motor neurons are involved in the control of movements.
Researchers from Ruhr-Universität Bochum have found that vitamin P works by sending the signals through another path than the molecule Brain Derived Neurotrophic Factor (BDNF) that was previously considered as important for the treatment of motor neuron disorders or after spinal cord damage.
"The Brain Derived Neurotrophic Factor only had a limited effect when tested on humans, and even had partially negative consequences", Prof. Dr. Stefan Wiese from the RUB Work Group for Molecular Cell Biology, said in a statement. "Therefore we are looking for alternative ways to find new approaches for the treatment of neurodegenerative diseases such as Amyotrophic Lateral Sclerosis."
BDNF stimulates two signaling pathways, the so-called MAP kinase and PI3K/AKT signal paths while researchers found that Vitamin P makes use only of the latter.
Researchers are of the opinion that vitamin P could have less negative effects than BDNF as vitamin P showed only positive effects on the motor neurons in less concentration range.
"These results show how important an accurate determination of dose and effect is", said Prof. Wiese. "It is easier to use, because vitamin P, in contrast to BDNF, can pass the blood-brain barrier and therefore does not have to be introduced into the cerebrospinal fluid using pumps like BDNF," Wiese added.
Tsai, T., Klausmeyer, A., Conrad, R., Gottschling, C., Leo, M., Faissner, A., & Wiese, S. (2013). 7,8-Dihydroxyflavone leads to survival of cultured embryonic motoneurons by activating intracellular signaling pathways Molecular and Cellular Neuroscience, 56, 18-28 DOI: 10.1016/j.mcn.2013.02.007... Read more »
Tsai, T., Klausmeyer, A., Conrad, R., Gottschling, C., Leo, M., Faissner, A., & Wiese, S. (2013) 7,8-Dihydroxyflavone leads to survival of cultured embryonic motoneurons by activating intracellular signaling pathways. Molecular and Cellular Neuroscience, 18-28. DOI: 10.1016/j.mcn.2013.02.007
Today (Tuesday 2 April 2013) is World Autism Awareness Day (WAAD).I don't exactly know how one is supposed to communicate this message ('Happy world autism awareness day' just doesn't roll off the tongue). So I guess all I will say is to reiterate the subtext of this blog on what the spectrum - the very wide spectrum - means: "To some it means a need for life-long support. To others it is part of the varied tapestry of humanity. To all it means a need to foster a welcoming society with appropriate support and opportunities."Onwards. Having discussed the latest paper from Drs Stephen Walker and Arthur Krigsman on bowel pathology in cases of autism potentially denoting a distinct condition from other inflammatory bowel diseases and stumbling upon the paper by Peeters and colleagues* on functional defecation disorder and autistic traits, I thought it appropriate to pop into the DeLorean and revisit a paper which never really received the recognition it deserved.The subject matter for today is the paper by Karoly Horvath and colleagues** published in 1999 as we begin another trip down the autism research memory lane, same as I did when covering the the Mary Goodwin paper from 1971 on the gut-brain axis and autism (see here) and the John Money autism and autoimmunity paper also from 1971 (see here).Hadrian's Wall @ Wikipedia Remember my nameThe name Karoly Horvath will probably be familiar to quite a few people who've been on the autism research scene for a while. Another of Dr Horvath's papers*** created a bit of stir a while back based on some very preliminary findings on the use of the digestive hormone, secretin for cases of autism.Following some initial reports of "transient, marginally significant improvements in autistic behaviors" in some cases as per studies like the one from Coniglio and colleagues****, a whole slew of subsequent trials have painted a rather less positive picture on the use of secretin for autism as per the review by Krishnaswami and colleagues***** (open-access) which quite emphatically stated that "secretin as a treatment approach for ASDs warrants no further study".I'm not one to normally challenge paper conclusions - particularly systematic reviews - but will perhaps contrast that quote with the closing remarks made by the Cochrane Library review of Williams and colleagues******. They left the secretin research door slightly ajar for those who were potentially able to identify "important subgroups of children with ASD who could benefit from secretin because of a proven link between the action of secretin and the known cause of their ASD, or the type of problems they are experiencing". I'm a great believer in subgroups when it comes to autism, or rather the autisms, and how a diagnosis of autism is seemingly protective of nothing when it comes to other conditions/states, so you can perhaps assume which quote was my preference.FactoidsAnyhow, back to the Horvath 1999 paper. A few interesting factoids from their report:Thirty-six children all diagnosed with an autism spectrum disorder (ASD), mean age 5.7 years, formed the participant group. Children were all referred to the gastroenterology (GI) clinic where the authors worked following the presence of various GI symptoms ranging from abdominal pain to chronic diarrhoea and various other presentations.As well as quite a bit of review of participants' medical history, various clinical investigations were undertaken which included a "full upper gastrointestinal workup", analysis of digestive enzyme function in the small intestine and some histological examination.Results: quite a few important findings. Reflux esophagitis was present in nearly 70% of participants (25/36). Chronic inflammation of the gastric mucosa was determined in 15 children. Reduced disaccharidase activity was present in approximately 60% of children, and in particular low lactase levels. Following administration of secretin, participants with autism and diarrhoea comorbid showed signs of increased pancreatico-biliary fluid output potentially indicative of "upregulation of the secretin receptors" itself potentially related to "either a defect in secretin production or a problem of release from the intestinal S cells"."There was no evidence of either fungal or bacterial overgrowth in the duodenum" was another finding.I know there is a lot to take in from those results so I'm going to try and put them into some kind of perspective with some of the other related literature in the peer-reviewed domain.Lactose intoleranceI'll start with the disaccharidase activity side of things. The Horvath results were in some respects ahead of their time with their findings in this area. I've talked previously about the Rafail Kushak paper and their findings of the frequency "of lactase deficiency was 58% in autistic children ≤ 5 years old and 65% in older patients". Notice the similarity in the percentages between Horvath and Kushak. Indeed, this whole area of carbohydrate malabsorption present in cases of autism was very nicely continued by the Brent Williams paper looking at enzyme activity and autism. I know a few people have talked about how some of these findings might overlap with for example, the various reports on the use and effectiveness of a gluten- and casein-free (cereal grains and mammalian dairy free) diet in some cases of autism. Certainly, I wouldn't rule out a possible overlap to account for any results.Reflux and GERDGastroesophageal reflux and reflux esophagitis - states pertaining to inflammation of the esophagus - were also commonly reported in the participant group and indeed also correlated with various behavioural manifestations noted in some cases (nighttime wakening, signs of irritability, abdominal discomfort) which are "typically reported by non-autistic children with esophagitis". A little reading around this topic suggests that many cases of such esophagitis are tied into things like GERD - gastroesophageal reflux disease - which is basically about stomach acid rising up instead of staying where it should be and causing damage. That being said, other explanations have also surfaced to potentially account for the damage done during GERD (see the paper by Souza and colleagues*******) highlighting a possible role for cytokines in this process. I'm also conscious of the findings of eosinophilic esophagitis being reported in individual cases of autism (see here). In terms of management options and without heading down any medical advice giving path, I was very interested to see a body of work appearing supporting the use of baclofen for cases of GERD********, a derivative of which - arbaclofen - has recently been touted as a potential intervention option for cases of autism. One has to wonder whether kum-ba-arbaclofen might be doing so much more than just affecting ... Read more »
Horvath K, Papadimitriou JC, Rabsztyn A, Drachenberg C, & Tildon JT. (1999) Gastrointestinal abnormalities in children with autistic disorder. The Journal of pediatrics, 135(5), 559-63. PMID: 10547242
What do you do if you drop your sandwich on the floor? Pick it up within five seconds and just continue eating? You’re not the only one. It’s a very convenient socially accepted code of behavior, but does it also make sense?... Read more »
Dawson, P., Han, I., Cox, M., Black, C., & Simmons, L. (2006) Residence time and food contact time effects on transfer of Salmonella Typhimurium from tile, wood and carpet: testing the five-second rule. Journal of Applied Microbiology, 2147483647. DOI: 10.1111/j.1365-2672.2006.03171.x
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