Showing posts with label memory. Show all posts
Showing posts with label memory. Show all posts

Tuesday, 7 May 2019

"...although their autistic traits were sometimes helpful, at other times they hindered their progress"

There's quite a lot of important information to be gleaned from the findings reported by Ginny Russell and colleagues [1] (open-access) following their questioning of autistic adults (or adults with autism if you prefer) about how they viewed themselves. How for example, said participants viewed their abilities and how "these abilities had helped them in their everyday lives: at work, in their relationships with other people, and at home" makes for interesting firsthand reading.

I have quite a lot of time for the primary author on this paper given other research she has produced (see here) and her recent involvement in an important paper that basically said what many people had been thinking for a while: autism research is typically biased against those who present with autism and intellectual (learning) disability [2]. That last research theme seems to have been something (partially) taken on board in this recent paper from Russell et al given their inclusion of voices from various 'parts' of the autism spectrum including those "receiving high-level support (living in full-time residential care)."

So: "All but one participant was able to describe their own traits and how these had benefited them, and the majority of participants could and did attribute these to autism." Various traits were discussed in the interviews (n=28) held with participants (n=24); key among them were "perceptual differences, memory, focus, and attention to detail, logic, and vivid imagination." Interview data / responses were also coded into various themes: "(1) experience of difference, (2) false dichotomies, and (3) moderating influences" which similarly provided further interesting data.

In relation to the 'experience of difference' we are told that this theme "encompassed how participants conceptualized the causes of their difference from “neurotypical” (NT) individuals." Although I am less than enamoured with the misnomer that is 'neurotypical' (see here for some discussions on how there is no single way for a brain to be 'normal') there is some important information contained in those accounts. Specifically how "most participants talked about autism as a set of qualities they possessed rather than an illness they had."

The theme of 'false dichotomies' was equally revealing as: "Participants gave accounts of traits as advantageous and simultaneously disadvantageous in the workplace, in relationships, and at home." The phrase 'double-edged sword' seems to be particularly apt when it came to the descriptions offered by participants in the Russell study; also denoting how: "There was no boundary between a strength and a weakness." This continues a theme from other research discussed recently (see here). Interestingly too under this category, some participants reported that: "there is no “autism—self” opposition... thus [they] saw their abilities and skills more holistically as generalized personality traits, which included autistic traits." Autistic traits as part of a wider picture eh?

The final theme - "Moderating influences" - also included some interesting data. Authors defined this as: "Factors that might determine whether a participant experienced a trait as advantageous or disadvantageous were classified as moderating influences." Perhaps unsurprisingly, social context was something mentioned in this theme, with examples like serving in the army or being incarcerated in prison being places where "a lack of empathy" and "sticking to routines" respectively, were seen as the right places to present such behaviours. Personally I'd quibble that a lack of empathy is a good place for the armed forces given that serving in active theatre is only part of the job but ho-hum. Another important part of the 'moderating influences' theme was the issue of 'controllability and extent'. As per my musings on the issue of 'stimming' and autism (see here again) this is probably the best example of that 'double-edged sword'. How things like focus, attention to detail and logic whilst all very positive traits, can sometimes become 'out of control' and cause all-manner of issues to a person.

There are of course caveats to the Russell findings, not least that their study reflected "a lack of severely intellectually and language-impaired participants" and so results cannot be generalised to everyone on the autism spectrum. Indeed they offer a solution: "Eliciting the opinions of these groups would require a different approach, perhaps observational" which really should be a research priority (see here). I'd also have been interested to see data on the comorbidity profile of the participant group too, bearing in mind that autism rarely appears in some sort of diagnostic vacuum (see here). And I'm also minded to mention that similar to other discussions on the 'positives' of other diagnostic labels (see here) one has to remember that autistic traits are not just something noted alongside a diagnosis of autism, and what this means when using emotive terms like "autistic advantage". This, particularly in the context that autism is diagnosed on the basis of traits significantly impinging on functioning and daily life (see here).

I suppose the bottom line from the Russell findings is summed up pretty well in their conclusions: "The findings make us wary of describing autistic advantages as fixed traits, rather their expression (and development) is context dependent." In other words, things like 'situation' influence whether a trait is seen as a deficit or an advantage. And just because a trait might initially be start out as an advantage or a deficit does not mean that it will necessarily stay that way across many different situations and various different time periods...

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[1] Russell G. et al. Mapping the Autistic Advantage from the Accounts of Adults Diagnosed with Autism: A Qualitative Study. Autism in Adulthood. 2019. Apr 3.

[2] Russell G. et al. Selection bias on intellectual ability in autism research: a cross-sectional review and meta-analysis. Mol Autism. 2019 Mar 1;10:9.

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Tuesday, 14 August 2018

Autistic traits carrying a 'cognitive cost' into old age?

I don't think anyone should be too alarmed at the findings reported by Gavin Stewart and colleagues [1]. But their observation that "autism traits as measured by the BAPQ [Broad Autism Phenotype Questionnaire] may confer additional risk of cognitive decline in aging" represents something that requires quite a bit of further investigation.

Some twenty 'older' adults who were questioned and deemed to have met criteria for the broader autism phenotype (BAP) were tested on skills related to executive function alongside episodic memory. Their results were compared with twenty 'older' adults who did not reach criteria for the BAP. Authors reported that: "Despite no differences in age, sex ratio, educational history or IQ, the BAP group demonstrated poorer performance on measures of executive function and episodic memory compared to the COA [control older adults] group." They interpret this in the context of that 'additional risk of cognitive decline in aging'.

The numbers of participants in the Stewart study were low and imply that one has to be quite careful about making any sweeping generalisations as a result. Bear also in mind that the BAP does not necessarily equal autism or autism spectrum disorder (ASD) as a function of it describing sub-threshold autistic traits (sub-threshold for a diagnosis). Traits, I might add, that are seemingly not just potentially representative of autism (see here for one example).

But set within a 'gap' in the research base looking at autism in older adults (see here), there is a scheme of work to follow. If for example, the Stewart 'trend' does overlap with the experiences of older adults on the autism spectrum in terms of 'cognitive decline', there is a whole barrage of potentially important implications to consider. More so when one considers that the autism prevalence data continues to head in only one direction (see here) and what this means for societal financial and resource planning.

Just before I go, one more detail was revealed in the Stewart paper: "Older adults who met the BAP criteria also reported higher levels of depression and anxiety." Continuing a theme on this blog that various over-represented issues/diagnoses in relation to autism might not be best described as just being 'comorbid' (see here and see here and see here), I believe that this finding adds further weight to the notion that autistic traits (clinical and sub-clinical) might have some important 'direct' relationships with other psychopathology. Not necessarily a welcome opinion in some quarters, but something that also requires a lot more investigation.

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[1] Stewart GR. et al. Aging with elevated autistic traits: Cognitive functioning among older adults with the broad autism phenotype. Research in Autism Spectrum Disorders. 2018; 54: 27-36.

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Wednesday, 23 March 2016

Antibiotic brain? Cognitive impairment by antibiotic-induced gut dysbiosis

"The present study shows that intragastric treatment of mice with an antibiotic mix impairs novel object recognition, but not spatial memory. This behavioral change is associated with a disruption of the microbial community in the colon, distinct alterations of the colonic and circulating metabolite profile and particular changes of neurochemical brain activity."

Those were the headlines attached to the paper published by Esther Fröhlich and colleagues [1] (open-access available here) who put further scientific flesh on the bones of the suggestion that those trillions of wee beasties (the gut microbiota) that call our gastrointestinal (GI) tract home, might be doing some much more than helping us digest our food or producing the odd nutrient or two. I say 'our' but should however point out that this was a study of mice not people.

Not content with the current evidence pertinent to establishing "causality in gut microbiota-brain relationships", researchers devised a plan to study various aspects of the effects of "antibiotic-induced gut dysbiosis" looking at the effects of an antibiotic mix on "(i) gut microbial community, (ii) metabolite profile in the colon, (iii) circulating metabolites, (iv) expression of neuronal signaling molecules in distinct brain areas and (v) cognitive behavior." All this carried out in adult mice, some of whom were given an antibiotic mix consisting of "ampicillin..., bacitracin..., meropenem..., neomycin... and vancomycin" who were then put through their paces with regards to a series of mouse cognitive tests before being sacrificed and further investigations carried out on their brain, blood and GI tract. I'll hasten to point out that I can't think of many typical occasions when such a combination of antibiotics together would be administered to people, so bear that in mind.

Results: well, first and foremost, authors were largely able to rule out any direct effect from the antibiotics themselves on brain function as a consequence of not detecting any metabolites of the antibiotics in the brains of those brave mouse participants. This despite the fact that "ampicillin had some oral bioavailability." Next, and as expected, the antibiotic mix "vigorously changed the microbiome." If you want some background on this, have a look at the interesting discussion piece on 'swallowing a grenade' from a while back (antibiotics not real grenades!). Researchers also reported that as a consequence of the disruption of normal gut bacterial service following antibiotic use, there was a shift in the types of metabolites produced by the surviving gut bacteria. So: "the levels of the short-chain fatty acids (SCFA) acetate, butyrate and propionate as well as of trimethylamine, adenine and uracil were significantly diminished by antibiotic treatment." This harks back to my opening sentiments about gut bacteria doing more than just helping digest food.

Next: "Antibiotic-treated mice had a significantly lower memory index than vehicle-treated mice."Vehicle-treated refers to those who did not receive the antibiotic mix. But, whilst one aspect of memory - novel object recognition - seemed to have been affected by antibiotic receipt, other aspects were seemingly not. The authors go on to report that various "neurochemical alterations" might be linked to the cognitive results reported including changes to "tight junction proteins, brain-derived neurotrophic factor, N-methyl-D-aspartate receptor subunit 2B, serotonin transporter, NPY system and corticosterone."

These are interesting findings and, as the authors conclude: "add to the understanding of the microbiota-gut-brain axis and highlight the potential and limitation of antibiotic-induced gut dysbiosis as model system to probe causality in the interaction between gut microbiota and brain." Accepting that there is a significant level of 'hype' around the possibility of a bacteria-gut-brain axis, this type of science is a welcome addition to the peer-reviewed literature and cries out for further independent replication.

Ideally, I would like to see a lot more research looking at the potentially important links between gut bacteria and behaviour in human participants. Obviously I'm not talking about dissecting people in the same way that Fröhlich et al sacrificed their mice, but I'm sure other study designs and methodologies could be introduced minus the need for death. Certainly the application of metabolomics to antibiotic use research could be quite revealing. Harking back to other research talking about toddler temperament potentially *correlating* with gut bacteria (see here) or even the extremes of psychosis appearing alongside acute urinary tract infection (see here), there are plenty of research avenues to pursue. The suggestion that recurrent antibiotic exposure might play some role in the experience of depression and/or anxiety (see here) would also seem to be as good a starting point if any when it comes to moving from mouse studies to human studies. Oh, and I'd minded to say that we might also want to look at gut barrier function too (see here)...

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[1] Fröhlich EE. et al. Cognitive Impairment by Antibiotic-Induced Gut Dysbiosis: Analysis of Gut Microbiota-Brain Communication. Brain Behav Immun. 2016 Feb 23. pii: S0889-1591(16)30040-X.

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ResearchBlogging.org Fröhlich EE, Farzi A, Mayerhofer R, Reichmann F, Jačan A, Wagner B, Zinser E, Bordag N, Magnes C, Fröhlich E, Kashofer K, Gorkiewicz G, & Holzer P (2016). Cognitive Impairment by Antibiotic-Induced Gut Dysbiosis: Analysis of Gut Microbiota-Brain Communication. Brain, behavior, and immunity PMID: 26923630