Offering multiple perspectives from many fields of human inquiry that may move all of us toward a more integrated understanding of who we are as conscious beings.
Here are a few links that have been hanging around in my browser for the last few days (or weeks). Hope you find them interesting - follow the title links to read the whole article.
By Gary Marcus, Adam Marblestone, and Jeremy Freeman
November 12, 2014
There is real reason to believe that the field is on the verge of a number of methodological breakthroughs: Soon we will be able to study the operation of the brain in unprecedented detail, yielding orders of magnitude more data than the field has ever seen before.
And that is a good thing. On virtually any account, neuroscience needs more data—a lot more data—than it has.
To begin with, we desperately need a parts list for the brain. The varied multitude of cells in the human brain have names like "pyramidal cells," "basket cells," and "chandelier cells," based on their physical structures. But we don’t know exactly how many cell types there are—some, like Cajal-Retzius cells (which play a role in brain development) are quite rare. And we know neither what all these different cell types do nor why there are so many. Until we have a fuller understanding of the parts list, we can hardly expect to understand how the brain as a whole functions.
A double exposure of weakly electric fish with recordings of brain activity. Credit Béatrice de Géa for The New York Times
James Gorman
November 10, 2014
Research on the brain is surging. The United States and the European Union have launched new programs to better understand the brain. Scientists are mapping parts of mouse, fly and human brains at different levels of magnification. Technology for recording brain activity has been improving at a revolutionary pace.
The National Institutes of Health, which already spends $4.5 billion a year on brain research, consulted the top neuroscientists in the country to frame its role in an initiative announced by President Obama last year to concentrate on developing a fundamental understanding of the brain.
Scientists have puzzled out profoundly important insights about how the brain works, like the way the mammalian brain navigates and remembers places, work that won the 2014 Nobel Prize in Physiology or Medicine for a British-American and two Norwegians.
Yet the growing body of data — maps, atlases and so-called connectomes that show linkages between cells and regions of the brain — represents a paradox of progress, with the advances also highlighting great gaps in understanding.
How light therapy can treat disorders from depression to Alzheimer’s disease.
By Katherine Hobson
November 20, 2014
ILLUSTRATION BY SHANNON FRESHWATER
Exactly how light works isn’t known, but many researchers suspect
that bright lights help SAD sufferers by regulating their sluggish
circadian clocks. Those clocks involve the suprachiasmatic nucleus, or
SCN, which is a small area of the brain’s hypothalamus that dictates the
rhythms of a host of bodily functions, including waking, sleeping, body
temperature, and alertness. Absent external cues, those rhythms
circulate for slightly longer than 24 hours for most people. (They
stabilized at 24:30 for a man who lived in a dark cave for two months.)
But normally these rhythms are harmonized with the external 24-hour
day/night cycle when light hits a cluster of special retinal cells that are sensitive to sunlight but not always involved with vision.
People
with SAD may have problems syncing their internal clocks in the winter,
such that darker mornings allow their body’s natural rhythms to drift
later. Exposure to an artificial bright light in the morning usually
improves their moods, says Lewy, presumably by changing the ebb and flow
of the stress hormone cortisol or other bodily processes orchestrated
by the SCN.
However, circadian rhythms appear to be disturbed in
non-seasonal maladies too, which means there is a potential for light
therapy beyond SAD, says Anna Wirz-Justice, professor emeritus at the
Psychiatric Hospital of the University of Basel. She adds that light
therapy has appeal for good reason. When it works, it does so
quickly—usually within a week or two. Also, the side effects appear to
be mild: Some patients have headaches or a slight nausea at the
beginning of treatment, and some report agitation. For researchers like
Wirz-Justice, the choice to use light rather than drugs for depression
and other mood disorders when possible is obvious. “Light is an active
pharmacological agent hitting the brain,” she says. But does it work?
Lester V. Bergman/Corbis - Feeding mice the bacterium Bacteroides fragilis can reverse autism-like symptoms.
Companies selling ‘probiotic’ foods have
long claimed that cultivating the right gut bacteria can benefit mental
well-being, but neuroscientists have generally been sceptical. Now there
is hard evidence linking conditions such as autism and depression to
the gut’s microbial residents, known as the microbiome. And
neuroscientists are taking notice — not just of the clinical
implications but also of what the link could mean for experimental
design.
“The field is going to another level of
sophistication,” says Sarkis Mazmanian, a microbiologist at the
California Institute of Technology in Pasadena. “Hopefully this will
shift this image that there’s too much commercial interest and data from
too few labs.”
This year, the US National
Institute of Mental Health spent more than US$1 million on a new
research programme aimed at the microbiome–brain connection. And on 19
November, neuroscientists will present evidence for the link in a
symposium at the annual Society for Neuroscience meeting in Washington
DC called ‘Gut Microbes and the Brain: Paradigm Shift in Neuroscience’.
In
a rare departure from technology and user-centered design topics, this
edition of the Namahn lecture series welcomed the world-renowned
biologist and primatologist Dr Frans de Waal, voted in 2011 by Discover as
among the 47 (all time) Great Minds of Science. De Waal’s work with
primates and other animals suggests that morality is neither man-made,
nor exclusive to us, but a consequence of evolution.
De Waal argues that morality is older than religion. All religion did
was appropriate innate human nature. Among people who do not believe in
evolution, many contest this view. In the US, where De Waal now lives,
Creationists believe that God created man, and that we only have
morality because of God. Even some American scientists claim that Moral
Law cannot be explained and will never be explained by evolutionary
biology.
This does not prevent Social Darwinists from applying so-called
Darwinist ideas (survival of the fittest) to society: "if you can’t
afford it, tough." But De Waal argues that the approach of these Social
Darwinists is incorrect: it does not correctly reflect either what
Darwin proved or our true nature as humans. If our ancestors had not
cooperated millions of years ago, we would not be where we are today.
Paul Whiteley, who blogs at Questioning Answers (mostly on autism research), posted this intriguing research summary from Progress in Neuro-Psychopharmacology and Biological Psychiatry on the relationship between the "gut-brain axis" and schizophrenia, which is not a new avenue of research, but is nonetheless still considered a fringe notion in the mainstream schizophrenia research.
It only makes sense that if we have an unhealthy microbiome (enteric nervous system), which we already know can cause depression, disease, and cognitive issues (a major symptom cluster in schizophrenia is cognitive distortion), then the entire system is at risk.
The full article is, of course, paywalled, but Whiteley offers a good, though too brief for me, summary of the study; and I have included the abstract from the original article.
A micropost to direct your attention to the recent paper by Katlyn Nemani and colleagues [1] titled: 'Schizophrenia and the gut-brain axis'. Mentioning words like that, I couldn't resist offering a little exposure to this review and opinion piece, drawing on what seems to be some renewed research interest in work started by pioneers such as the late Curt Dohan [2].
The usual triad of gastrointestinal (GI) variables - gut barrier, gut bacteria and gut immune function - are mentioned in the article, concluding that: "A significant subgroup of patients may benefit from the initiation of a gluten and casein-free diet" among other things. Not a million miles away from related suggestions when it comes to something like the autism spectrum disorders (ASDs) (see here) bearing in mind the concept of overlapping spectrums (see here) and the [plural] schizophrenias. I'm also minded to hat-tip another research team including Emily Severance and colleagues who are going great guns when it comes to the whole GI-food link in cases of schizophrenia and beyond (see here for my recent discussion of some of her work). Another of her quite recent papers [3] on cerebrospinal fluid (CSF) levels of antibody response to wheat gluten and bovine milk in first-episode schizophrenia represents another master-class of research in this area. Their suggestion of potential evidence for a leaky blood-CSF barrier is something else which might stimulate further research in this area including some mention for the molecular handyperson that is melatonin among other things to "protect against blood-brain barrier and choroid plexus pathologies". Such findings might also be relevant for other CSF issues reported with schizophrenia in mind (see here). And whilst we're talking all-things biological membrane permeability and schizophrenia, I'll also link to the paper by Julio-Pieper and colleagues [4] (open-access) reviewing some of the evidence on the 'controversial association' between intestinal barrier dysfunction and various conditions (also covering some of the literature with autism in mind too). Mainstream here we come?
---------- [1] Nemani K. et al. Schizophrenia and the gut-brain axis. Prog Neuropsychopharmacol Biol Psychiatry. 2014 Sep 17. pii: S0278-5846(14)00168-7 [2] Dohan FC. Cereals and schizophrenia data and hypothesis. Acta Psychiatrica Scandinavica. 1966; 42: 125–152. [3] Severance EG. et al. IgG dynamics of dietary antigens point to cerebrospinal fluid barrier or flow dysfunction in first-episode schizophrenia. Brain Behav Immun. 2014 Sep 17. pii: S0889-1591(14)00462-0. [4] Julio-Pieper M. et al. Review article: intestinal barrier dysfunction and central nervous system disorders - a controversial association. Aliment Pharmacol Ther. 2014 Sep 28.
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Nemani, K., Ghomi, R., McCormick, B., & Fan, X. (2014). Schizophrenia and the gut–brain axis. Progress in Neuro-Psychopharmacology and Biological Psychiatry. 56(2): 155–160. DOI: 10.1016/j.pnpbp.2014.08.018
Several risk factors for the development of schizophrenia can be linked through a common pathway in the intestinal tract
The microbiota composition may impact the gastrointestinal barrier, immune regulation, and metabolism seen in schizophrenia.
A significant subgroup of patients may benefit from the initiation of a gluten and casein-free diet
Antimicrobials and probiotics have therapeutic potential that will be elucidated by further research
Abstract Several risk factors for the development of schizophrenia can be linked through a common pathway in the intestinal tract. It is now increasingly recognized that bidirectional communication exists between the brain and the gut that uses neural, hormonal, and immunological routes. An increased incidence of gastrointestinal (GI) barrier dysfunction, food antigen sensitivity, inflammation, and the metabolic syndrome is seen in schizophrenia. These findings may be influenced by the composition of the gut microbiota. A significant subgroup of patients may benefit from the initiation of a gluten and casein-free diet. Antimicrobials and probiotics have therapeutic potential for reducing the metabolic dysfunction and immune dysregulation seen in patients with schizophrenia.
