Which communities deserve your membership?

This 2015 California/Oxford review described the interplay between an individual and their group membership from an evolutionary biology viewpoint:

“Many central questions in evolutionary biology rely on understanding how individual-level and group-level selective processes interact to shape phenotypic variation and specialisation. Individuals can aggregate into groups, and the composition of these groups, populations, or communities (herein group phenotypic composition or GPC) can affect group-level dynamics and self-organisation.

Research across a range of disparate topics will benefit from simultaneously developing an understanding of how GPC affects individual fitness [genetic fitness, not physical fitness] and exerts selection on individual phenotypes, and assessing how individual phenotypes respond to GPC.

GPC can be a function of the phenotypes of its members or an emergent property that is not attributable to any single individual, such as the mating system. GPC is also an emergent property of genotypes and their patterns of expression.

GPC can affect individual fitness by influencing the overall performance of the group on collective tasks, affecting all the members of any given group equally, or by affecting the relative performance of different phenotypes within groups. For instance, a group with more aggressive individuals can be more successful at foraging, but aggressive individuals can have a higher fitness than non-aggressive individuals because they can monopolise a larger share of the total resources.

Individuals can respond to the effect of GPC by altering the phenotypic composition of the group (for example by controlling access to the group) and/or by changing their own phenotype.”

See my Individual evolution page for more on the topic of human individuals “changing their own phenotype.”

The review provided specific examples to illustrate each point of the overall framework. The authors seldom mentioned human examples, although many of the discussion items applied. Two of their points that weren’t necessarily applicable to human groups were:

  • Benefits from reducing competition
  • Altruism wasn’t viewed as an individual trait.

The authors didn’t use human-specific examples in their framework. For example, they mentioned division of labor, which benefits both animals and humans. There was no mention of applying capital to efforts, which is thought to be specific to humans, although reuse of tools by crows and chimpanzees may be animal examples.

I’d guess that the authors didn’t refer to humans often because that may have added the human trait of unforced individual choice. Unlike other species, we have the capability to direct much of our own lives, and choose the communities to which we belong.

A few questions about our group membership decisions:

  • Do we choose group memberships based on how the group recognizes and facilitates the unique individual each of us is?
  • How do we benefit as an individual when we become default members of communities by not making choices?
  • What individual benefits may we receive by opting out of default groups?

http://www.sciencedirect.com/science/article/pii/S0169534715001846 “From Individuals to Groups and Back: The Evolutionary Implications of Group Phenotypic Composition”

The mystery of humans’ evolved capability for adults to grow new brain cells

This 2016 German review discussed the evolution of human adult neurogenesis:

“Mammalian adult hippocampal neurogenesis is a trait shaped by evolutionary forces that have contributed to the advantages in natural selection that are associated with the mammalian dentate gyrus. Adult hippocampal neurogenesis in mammals originates from an ectopic precursor cell population that resides in a defined stem-cell niche detached from the ventricular wall.

Neurogenesis in the adult olfactory bulb generates a diverse range of interneurons, and is involved in the processing of sensory input. In contrast, adult hippocampal neurogenesis produces only one type of excitatory principal neuron and plays a role in flexible memory formation.

A surplus of new neurons is generated first from which only a subset survives. And it is exactly these new neuronal nodes that, at least for a transient period, are the carriers of synaptic plasticity.

For a number of weeks after they were born, the new neurons have a lower threshold for long-term potentiation. This directs the action to the new cells and results in a bias toward the most plastic cells in the local circuitry.

It is a highly polygenic trait, and numerous genes have already been identified to ultimately have essentially identical effects on net neurogenesis.

Adult neurogenesis is also an individualizing trait. Even before an identical genetic background, subtle individual differences in starting conditions and differential behavioral trajectories result in an increase in phenotypic variation with time.”

The author continued the penultimate paragraph above to pose a question about adult neurogenesis that’s incompletely answered by evolutionary biology theory and evidence todate:

“How genetic variation in single genes (or many genes) would be able to exert a phenotypic change in neurogenesis that can provide a large enough advantage to be selected for.”

The development of new brain cells throughout our lives helps us continually adapt and learn. The “increase in phenotypic variation with time” helps us maintain the unique individual that each of us is.

The review emphasized to me how “individual differences” should neither be viewed as a mystery, nor explained away, nor treated as an etiological factor as researchers often do. Focusing on what caused the differences may provide clearer information.

http://cshperspectives.cshlp.org/content/8/2/a018986.full “Adult Neurogenesis: An Evolutionary Perspective”

A problematic study of oxytocin receptor gene methylation, childhood abuse, and psychiatric symptoms

This 2016 Georgia human study found:

“A role for OXTR [oxytocin receptor gene] in understanding the influence of early environments on adult psychiatric symptoms.

Data on 18 OXTR CpG sites, 44 single nucleotide polymorphisms, childhood abuse, and adult depression and anxiety symptoms were assessed in 393 African American adults. The Childhood Trauma Questionnaire (CTQ), a retrospective self-report inventory, was used to assess physical, sexual, and emotional abuse during childhood.

While OXTR CpG methylation did not serve as a mediator to psychiatric symptoms, we did find that it served as a moderator for abuse and psychiatric symptoms.”

From the Limitations section:

  1. “Additional insight will likely be gained by including a more detailed assessment of abuse timing and type on the development of biological changes and adverse outcomes.
  2. The degree to which methylation remains fixed following sensitive developmental time periods, or continues to change in response to the environment, is still a topic of debate and is not fully known.
  3. Comparability between previous findings and our study is limited given different areas covered.
  4. Our study was limited to utilizing peripheral tissue [blood]. OXTR methylation should ideally be assessed in the tissues that are known to express OXTR and directly involved in psychiatric symptoms. The degree to which methylation of peripheral tissues can be used to study methylation changes in response to the environment or in association with behavioral outcomes is currently a topic of debate.
  5. Our study did not evaluate gene expression and thus cannot explore the role of study CpG sites on regulation and expression.”

Addressing the study’s limitations:

  1. Early-life epigenetic regulation of the oxytocin receptor gene demonstrated – with no hint of abuse – how sensitive an infant’s experience-dependent oxytocin receptor gene DNA methylation was to maternal care. Treating prenatal stress-related disorders with an oxytocin receptor agonist provided evidence for prenatal oxytocin receptor gene epigenetic changes.
  2. No human’s answers to the CTQ, Adverse Childhood Experiences, or other questionnaires will ever be accurate self-reports of their prenatal, infancy, and early childhood experiences. These early development periods were likely when the majority of the subjects’ oxytocin receptor gene DNA methylation took place. The CTQ self-reports were – at best – evidence of experiences at later times and places, distinct from earlier experience-dependent epigenetic changes.
  3. As one example of incomparability, the 2009 Genomic and epigenetic evidence for oxytocin receptor deficiency in autism was cited in the Introduction section and again in the Limitations section item 4. Since that study was sufficiently relevant to be used as a reference twice, the researchers needed to provide a map between its findings and the current study.
  4. Early-life epigenetic regulation of the oxytocin receptor gene answered the question of whether or not an individual’s blood could be used to make inferences about their brain oxytocin receptor gene DNA methylation. The evidence said: NO, it couldn’t.
  5. It’s assumed that oxytocin receptor gene DNA methylation directly impacted gene expression such that increased levels of methylation were associated with decreased gene transcription. The study assumed but didn’t provide evidence that higher levels of methylation indicated decreased ability to use available oxytocin due to decreased receptor expression. The study also had no control group.

To summarize the study’s limitations:

  1. The study zeroed in on childhood abuse, and disregarded evidence for more relevant factors determining an individual’s experience-dependent oxytocin receptor gene DNA methylation. That smelled like an agenda.
  2. The study used CTQ answers as determinants, although what happened during the subjects’ earliest life was likely when the majority of epigenetic changes to the oxytocin receptor gene took place. If links existed between the subjects’ early-life DNA methylation and later-life conditions, they weren’t evidenced by CTQ answers about later life that couldn’t self-report relevant experiences from conception through age three that may have caused DNA methylation.
  3. There was no attempt to make findings comparable with cited studies. That practice and the lack of a control group reminded me of Problematic research with telomere length.
  4. The researchers tortured numbers until they confessed “that CpG methylation may interact with abuse to predict psychiatric symptoms.” But there was no direct evidence that each subject’s blood oxytocin gene receptor DNA methylation interacted as such! Did the “may interact” phrase make the unevidenced inferences more plausible, or permit contrary evidence to be disregarded?
  5. See Testing the null hypothesis of oxytocin’s effects in humans for examples of what happens when researchers compound assumptions and unevidenced inferences.

The study’s institution, Emory University, and one of the study’s authors also conducted Conclusions without evidence regarding emotional memories. That 2015 study similarly disregarded relevant evidence from other research, and made statements that weren’t supported by that study’s evidence.

The current study used “a topic of debate” and other disclaimers to provide cover for unconvincing methods and analyses in pursuit of..what? What overriding goals were achieved? Who did the study really help?

http://onlinelibrary.wiley.com/enhanced/doi/10.1111/cdev.12493/ “Oxytocin Receptor Genetic and Epigenetic Variations: Association With Child Abuse and Adult Psychiatric Symptoms”

This post has somehow become a target for spammers, and I’ve disabled comments. Readers can comment on other posts and indicate that they want their comment to apply here, and I’ll re-enable comments.

Early-life epigenetic regulation of the oxytocin receptor gene

This 2015 US/Canadian rodent study investigated the effects of natural variation in maternal care:

“The effects of early life rearing experience via natural variation in maternal licking and grooming during the first week of life on behavior, physiology, gene expression, and epigenetic regulation of Oxtr [oxytocin receptor gene] across blood and brain tissues (mononucleocytes, hippocampus, striatum, and hypothalamus).

Rats reared by high licking-grooming (HL) and low licking-grooming (LL) rat dams exhibited differences across study outcomes:

  • LL offspring were more active in behavioral arenas,
  • Exhibited lower body mass in adulthood, and
  • Showed reduced corticosterone responsivity to a stressor.

Oxtr DNA methylation was significantly lower at multiple CpGs in the blood of LL versus HL males, but no differences were found in the brain. Across groups, Oxtr transcript levels in the hypothalamus were associated with reduced corticosterone secretion in response to stress, congruent with the role of oxytocin signaling in this region.

Methylation of specific CpGs at a high or low level was consistent across tissues, especially within the brain. However, individual variation in DNA methylation relative to these global patterns was not consistent across tissues.

These results suggest that:

  • Blood Oxtr DNA methylation may reflect early experience of maternal care, and
  • Oxtr methylation across tissues is highly concordant for specific CpGs, but
  • Inferences across tissues are not supported for individual variation in Oxtr methylation.


Individual DNA methylation values were not correlated across brain tissues, despite tissue concordance at the group level.

For each CpG, we computed the Pearson correlation coefficient r between methylation values for matched samples in pairs of brain regions (bars). Dark and light shaded regions represent 95% and 99% thresholds, respectively, of distributions of possible correlation coefficients determined from 10,000 permutations of the measured values among the individuals. These distributions represent the null hypothesis that an individual DNA methylation value in one brain region does not help to predict the value in another region in the same animal.

(A) Correlations based on pyrosequencing data for matched samples passing validation in both hippocampus (HC) and hypothalamus (Hypo). Correlations for individuals at each CpG were either weak (.2 < r < .3) or absent (r < .2), and none were significant, even prior to correction for multiple comparisons.

(B) Correlations for matched samples passing validation in both hippocampus and striatum (Str). Two correlations (CpG 1 and 11) were individually significant prior to but not following correction, and this result could be expected by chance.

Correlations between hippocampus and blood (described in the text) yielded similar results, and no particular CpG yielded consistently high correlation across multiple tissues.”

The study focused on whether or not an individual’s experience-dependent oxytocin receptor gene DNA methylation in one of the four studied tissues could be used to infer a significant effect in the three other tissues. The main finding was NO, it couldn’t!

The researchers’ other findings may have been strengthened had they also examined causes for the observed effects. The “natural variation in maternal licking and grooming” developed from somewhere, didn’t it?

The subjects’ mothers were presumably available for the same tests as the subjects, but nothing was done with them. Investigating at least one earlier generation may have enabled etiologic associations of “the effects of early life rearing experience” and “individual variation in DNA methylation.”

https://www.sciencedirect.com/science/article/abs/pii/S0018506X1500118X “Natural variation in maternal care and cross-tissue patterns of oxytocin receptor gene methylation in rats” (not freely available)

Does vasopressin increase mutually beneficial cooperation?

This 2016 German human study found:

“Intranasal administration of arginine vasopressin (AVP), a hormone that regulates mammalian social behaviors such as monogamy and aggression, increases humans’ tendency to engage in mutually beneficial cooperation.

AVP increases humans’ willingness to cooperate. That increase is not due to an increase in the general willingness to bear risks or to altruistically help others.”

One limitation of the study was that the subjects were all males, ages 19-32. The study’s title was “human risky cooperative behavior” while omitting subjects representing the majority of humanity.

Although the researchers claimed brain effects from vasopressin administration, they didn’t provide direct evidence for the internasally administered vasopressin in the subjects’ brains. A similar point was made about studies of vasopressin’s companion neuropeptide, oxytocin, in Testing the null hypothesis of oxytocin’s effects in humans.

A third limitation was that although the researchers correlated brain activity with social behaviors, they didn’t carry out all of the tests necessary to demonstrate the claimed “novel causal evidence for a biological factor underlying cooperation.” Per Confusion may be misinterpreted as altruism and prosocial behavior, the researchers additionally needed to:

“When attempting to measure social behaviors, it is not sufficient to merely record decisions with behavioral consequences and then infer social preferences. One also needs to manipulate these consequences to test whether this affects the behavior.”

http://www.pnas.org/content/113/8/2051.full “Vasopressin increases human risky cooperative behavior”

The effects of imposing helplessness

This 2016 New York rodent study found:

“By using unbiased and whole-brain imaging techniques, we uncover a number of cortical and subcortical brain structures that have lower activity in the animals showing helplessness than in those showing resilience following the LH [learned helplessness] procedure. We also identified the LC [locus coeruleus] as the sole subcortical area that had enhanced activity in helpless animals compared with resilient ones.

Some of the brain areas identified in this study – such as areas in the mPFC [medial prefrontal cortex], hippocampus, and amygdala – have been previously implicated in clinical depression or depression-like behavior in animal models. We also identified novel brain regions previously not associated with helplessness. For example, the OT [olfactory tubercle], an area involved in odor processing as well as high cognitive functions including reward processing, and the Edinger–Westphal nucleus containing centrally projecting neurons implicated in stress adaptation.

The brains of helpless animals are locked in a highly stereotypic pathological state.”

Concerning the study’s young adult male subjects:

“To achieve a subsequent detection of neuronal activity related to distinct behavioral responses, we used the c-fosGFP transgenic mice expressing c-FosGFP under the control of a c-fos promoter. The expression of the c-fosGFP transgene has been previously validated to faithfully represent endogenous c-fos expression.

Similar to wild-type mice, approximately 22% (32 of 144) of the c-fosGFP mice showed helplessness.”

The final sentence of the Introduction section:

“Our study..supports the view that defining neuronal circuits underlying stress-induced depression-like behavior in animal models can help identify new targets for the treatment of depression.”

Helplessness is both a learned behavior and a cumulative set of experiences during every human’s early life. Therapeutic approaches to detrimental effects of helplessness can be different with humans than with rodents in that we can address causes.

The researchers categorized activity in brain circuits as causal in the Discussion section:

“Future studies aimed at manipulating these identified neural changes are required for determining whether they are causally related to the expression of helplessness or resilience.”

Studying whether or not activity in brain circuits induces helplessness in rodents may not inform us about causes of helplessness in humans. Our experiences are often the ultimate causes of helplessness effects. Many of our experiential “neural changes” are only effects, as demonstrated by this and other studies’ induced phenotypes such as “Learned Helplessness” and “Prenatally Restraint Stressed.”

Weren’t the researchers satisfied that the study confirmed what was known and made new findings? Why attempt to extend animal models that only treat effects to humans, as implied in the Introduction above and in the final sentence of the Discussion section:

“Future studies aimed at elucidating the specific roles of these regions in the pathophysiology of depression as well as serve as neural circuit-based targets for the development of novel therapeutics.”

http://journal.frontiersin.org/article/10.3389/fncir.2016.00003/full “Whole-Brain Mapping of Neuronal Activity in the Learned Helplessness Model of Depression” (Thanks to A Paper a Day Keeps the Scientist Okay)

Does shame keep you up at night?

This 2016 Netherlands human study found:

“Restless REM [rapid eye movement] sleep reflects a process that interferes with the overnight resolution of distress. Its accumulation may promote the development of chronic hyperarousal.

We use the term “restless REM sleep” here to refer to REM sleep with a high number of phasic events, including arousals and eye movements.

The present study focused on shame, because it may interfere the most with healthy psychological functioning and was shown to be predictive of developing depression and PTSD symptoms, including hyperarousal. By obstructing effective coping mechanisms, shame often hinders therapeutic progress, to the point that it may even lead to a negative therapeutic outcome.

A dedicated assessment of the subjective duration of distress after a shameful experience was complemented by assessments on nocturnal mentation, insomnia severity, hyperarousal, and major life events, as well as an Internet-implemented structured interview on health.”

From the Limitations section:

  1. “Restless REM sleep was not directly quantified but approximated by means of a validated questionnaire rating of thought-like nocturnal mentation.
  2. Non-REM sleep has also been implicated in the resolution of emotional distress.
  3. A third limitation regards the observational nature of the present study..a more definite conclusion will require studies using experimental manipulation of emotions and sleep.
  4. Whereas there was good reason to focus first on distress induced by shame in our innovative approach to the role of sleep in self-conscious emotions rather than the basic emotions usually studied, our findings should not be interpreted as supporting a unique role for shame or self-conscious emotions. Future studies could address whether the duration of distress elicited by other self-conscious and basic emotions has a similar two-factor structure.”

I applaud the inclusion of emotion in research. I’m not convinced that studying shame will lead to etiologic advances in science, though.

How does shame arise in our lives? Is it a biologic human need on the same level as nourishment, protection, and socialization?

Shame is a symptom along with “nocturnal mentation, insomnia severity, hyperarousal.” If a person’s thoughts, feelings, behavior, and sleep are adversely affected by shame, a resolution should be achieved by addressing the underlying causes, not by tamping down the symptoms.

http://www.pnas.org/content/113/9/2538.full “Slow dissolving of emotional distress contributes to hyperarousal”

Telomerase activity outside of telomere maintenance

This 2016 Singapore review was on the role of telomerase in cancers. From its background section:

“Telomeres are conserved, repetitive sequences located at the ends of eukaryotic chromosomes which protect the integrity of genomic DNA. DNA polymerase is unable to replicate the 5′ [carbon number] ends of chromosomes, hence, cells require a RNA dependent DNA polymerase called telomerase to synthesize DNA on the lagging strand. Telomerase activity is tightly regulated and seen mainly in germ cells, stem cells and some immune cell types which have high proliferative needs.

In contrast, somatic cells do not display detectable telomerase activity. As a result, the chromosomes of normal somatic cells shorten 50–200 bp [base pair] each replication at the telomeres due to the problem of end replication. Thus, somatic cells are eventually burdened with DNA damage, replication crisis, cellular senescence or apoptosis and can divide only limited number of times, whereas cells that have active telomerase possess unlimited proliferative potential.”

The main section of the review described the details of how:

“Reactivation of telomerase has been considered as a strategy for telomere maintenance and is a major hallmark of cancer. Although the major function of telomerase is thought to be telomere elongation, accumulating evidence has suggested that it can modulate expression of various genes which affect cancer progression and tumorigenesis.”

http://link.springer.com/article/10.1007/s00018-016-2146-9/fulltext.html “Reactivation of telomerase in cancer”

Advance science by including emotion in research

This 2015 analysis of emotion studies found:

“Emotion categories [fear, anger, disgust, sadness, and happiness] are not contained within any one region or system, but are represented as configurations across multiple brain networks.

For example, among other systems, information diagnostic of emotion category was found in both large, multi-functional cortical networks and in the thalamus, a small region composed of functionally dedicated sub-nuclei.

The dataset consists of activation foci from 397 fMRI and PET [positron emission tomography] studies of emotion published between 1990 and 2011.”

From the fascinating Limitations section:

“Our analyses reflect the composition of the studies available in the literature, and are subject to testing and reporting biases on the part of authors. This is particularly true for the amygdala (e.g., the activation intensity for negative emotions may be over-represented in the amygdala given the theoretical focus on fear and related negative states). Other interesting distinctions were encoded in the thalamus and cerebellum, which have not received the theoretical attention that the amygdala has and are likely to be bias-free.

Some regions—particularly the brainstem—are likely to be much more important for understanding and diagnosing emotion than is apparent in our findings, because neuroimaging methods are only now beginning to focus on the brainstem with sufficient spatial resolution and artifact-suppression techniques.

We should not be too quick to dismiss findings in ‘sensory processing’ areas, etc., as methodological artifacts. Emotional responses may be inherently linked to changes in sensory and motor cortical processes that contribute to the emotional response.

The results we present here provide a co-activation based view of emotion representation. Much of the information processing in the brain that creates co-activation may not relate to direct neural connectivity at all, but rather to diffuse modulatory actions (e.g., dopamine and neuropeptide release, much of which is extrasynaptic and results in volume transmission). Thus, the present results do not imply direct neural connectivity, and may be related to diffuse neuromodulatory actions as well as direct neural communication.”

Why did the researchers use only 397 fMRI and PET studies? Why weren’t there tens or hundreds of times more candidate studies from which to select?

The relative paucity of candidate emotion studies demonstrated the prevalence of other researchers’ biases for cortical brain areas. The lead researcher of the current study was a coauthor of the 2016 Empathy, value, pain, control: Psychological functions of the human striatum, whose researchers mentioned that even their analyses of 5,809 human imaging studies was hampered by other imaging-studies researchers’ cortical biases.

Functional MRI signals depend on the changes in blood flow that follow changes in brain activity. Study designers intentionally limit their findings when they scan brain areas and circuits that are possibly activated by human emotions, yet exclude emotional content that may activate these areas and circuits.

Here are a few examples of limited designs that led to limited findings when there was the potential for so much more:

It’s well past time to change these practices now in the current year.

This study provided many methodological tests that should be helpful for research that includes emotion. It showed that there aren’t impenetrable barriers – other than popular memes, beliefs, and ingrained dogmas – to including emotional content in studies.

Including emotional content may often be appropriate and informative, with the resultant findings advancing science. Here are a few recent studies that did so:

http://journals.plos.org/ploscompbiol/article?id=10.1371%2Fjournal.pcbi.1004066 “A Bayesian Model of Category-Specific Emotional Brain Responses”

Publicly-funded researchers need to provide unqualified free access to their studies

A magazine article New Clues to How the Brain Maps Time reviewed the findings of a 2015 Boston rodent study During Running in Place, Grid Cells Integrate Elapsed Time and Distance Run. The article’s information was mixed such that when the reader arrived at this phrase:

“Moreover, time cells rely on context; they only mark time when the animal is put into a situation in which time is what matters most.”

it wasn’t clear whether the “time cells” referred to grid cells located in the entorhinal cortex (per the referenced study) or some other cells located in the hippocampus.

The hippocampus also has “time cells.” One of the first studies I curated when I started this blog one year ago today was Our memories are formed within a specific context. That 2014 study’s Significance section included:

“A number of recent studies have shown that the hippocampus, a structure known to be essential to form episodic memories, possesses neurons that explicitly mark moments in time.

We add a previously unidentified finding to this work by showing that individual primate hippocampal neurons not only track time, but do so only when specific contextual information (e.g., object identity/location) is cued.”

I attempted to disambiguate the “time cells” location by reading the 2015 study, only to find it was behind a paywall for which the public doesn’t have unqualified free access.

I assert that the study was performed using public funds, and that the researchers’ infrastructure and facilities were paid in part by the US taxpayers. Only US government funding sources were disclosed on the organization Mission Statement page of the study’s lead researcher, whose position is Lab Chief.

I assume that whether or not the study had unqualified free access was the researchers’ decision. Here’s a typical US NIH statement:

“The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.”

There are multiple problems with placing publicly-funded studies behind paywalls. One pertinent to this study and article was the accurate presentation of the study’s findings in news coverage.

The article’s author gave her interpretation of the study and the lead researcher’s remarks. She solicited five other researchers’ opinions, and one researcher provided an appraisal in the Comments section.

Was this treatment of the study’s findings sufficient for the public to understand what the US taxpayers paid for?

It was nice to have interpretations and remarks and opinions and appraisals, but these may have diverged from what the study actually found. Without unqualified free access to the study, there was no base on which to compare and contrast the article’s POVs.

Other news coverage of the study provided further examples of why publicly funded research needs to be freely available without qualification:

  • NPR’s coverage also confused the cells’ location: “If grid cells in the hippocampus and entorhinal cortex..”
  • An article carried by multiple sites headlined the cells as Odometer neurons.” Did the study find that grid cells operated cumulatively like an odometer that began at some stage of the subjects’ development? Or did it find that the grid cells operated more like a trip meter?
  • In the Discover Magazine coverage the lead researcher stated: “..could point to ways to treat memory loss, whether from old age or illness, like Alzheimer’s disease.” Did the study actually find anything about “memory loss?” Was there anything in it about “old age or illness, like Alzheimer’s disease?”

As the study’s news coverage discrepancies and ambiguities demonstrated, there’s every reason for researchers to provide all the details of their work. We’re well past the days when “wise old men” selectively gate information flows.