7/11/22, 8:52 AM What We Can Learn from Mouse Models of Autism

A mouse is seen in a plastic box at the Laboratory Animal Services Center (LASC) of the University of Zurich in
Schlieren, Switzerland, on Feb. 07, 2022. (Arnd Wiegmann/Reuters)

PREMIUM HEALTH VIEWPOINTS

What We Can Learn from Mouse

Models of Autism
BY STEPHANIE SENEFF TIME MARCH 28, 2022
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Autism is a complex neurodevelopmental disorder whose incidence has been

rising dramatically in the past two decades, in step with the dramatic rise in
the use of glyphosate (the active ingredient in the pervasive herbicide
Roundup) on core food crops [1, 2]. While correlation does not necessarily
mean causation, there are multiple mechanisms by which glyphosate’s
disruption of human biology, and the biology of the gut microbiome, could
cause many of the observed symptoms and biological metrics associated
with autism [3, 4].

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Remarkably, mice can acquire a syndrome that looks a great deal like human
autism, and researchers have been able to create multiple breeds of “designer
mice” that exhibit autism–like socio–communicative deficits. These mouse
strains have turned out to be very useful for helping us understand the
pathology of human autism, even though the mapping is not perfect. One
such strain is a naturally occurring inbred strain known as BTBR T+tf/J mice
(BTBR for short) [5, 6]. Another mouse model was generated by exposing a
mouse dam’s brain to a toxic chemical emulating a viral infection during
gestation, and this resulted in the expression of autism–like behaviors in
many of the pups [7, 8, 17]. In what is perhaps the most surprising experiment
due to its specificity, researchers were able to create autism in mice simply by
eliminating their brain’s ability to produce an important biological molecule
called heparan sulfate, by inactivating, only in the brain, a gene that encodes a
specific enzyme that is essential for its synthesis [9]. This manipulation was
done at birth. The authors wrote in the paper: “Remarkably, these mutant
mice recapitulate almost the full range of autistic symptoms, including
impairments in social interaction, expression of stereotyped, repetitive
behavior, and impairments in ultrasonic vocalization.” Many of the unique
features that show up in these mouse models, particularly with respect to
disruption of the gut microbes, have parallels among autistic children.

Glyphosate is used extensively in agriculture, both on genetically engineered

Roundup–Ready crops and on other core crops, such as wheat and sugar
cane, as a desiccant just before harvest. Our food supply is highly
contaminated with glyphosate, and so many children in America are exposed
daily to this toxic chemical. The latest number coming from the Centers for
Disease Control on autism rates in the U.S. is one out of every 44 children as
of 2021, higher than any previous year.

Heparan Sulfate and the Brain Ventricles

The fact that a manipulation so specific to heparan sulfate in the brain is

enough to induce autism in mice suggests that brain deficiencies in heparan
sulfate may be a key central pathology in human autism. Indeed, many
genetic mutations linked to autism involve enzymes associated with the
synthesis of the so–called extracellular matrix [10]. This is the non–cellular
component of tissues and organs, which not only provides physical
scaffolding but also initiates and orchestrates many biomechanical and
biochemical cues that govern cell physiological responses to environmental
stimulants [11]. A number of the mutations linked to human autism occur in a
set of genes that are called “glycogenes,” which encode the proteins and lipids
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that are bound to heparan sulfate in the matrix, forming “heparan sulfate
proteoglycans” (HSPGs), or enzymes involved in “glycosylation” – the binding
of heparan sulfate and similar complex sugar chain molecules to these
proteins and lipids [10].

The ventricles of the brain are a network of cavities in the middle of the brain
that are filled with cerebrospinal fluid. Heparan sulfate (HS) is prominent in
the ventricles, found within structures called “fractones,” making up the stem
cell niche that initiates neurogenesis [12]. Under the guidance of HSPGs
within these specialized extracellular matrix zones, stem cells proliferate and
differentiate into specialized cells and migrate into the brain to replace
damaged neurons. Studies on mice have shown that disruption of an enzyme
that is essential for synthesis of HS in the early developmental stages of mouse
embryos results in severe disruption of brain development [13].

I mentioned earlier the inbred BTBR breed of mice that have been extensively
studied because of their autistic profile [5, 6, 14]. Just like the mice with
disrupted HS synthesis in the brain, these BTBR mice also exhibit HS
deficiency in the brain [14]. The morphological development of the brain
appears normal, with the big exception that it is missing the corpus callosum,
a thick band of nerve fibers that connects the left and right sides of the brain
and forms a roof over the ventricles. It consists of tightly packed tracks of
white matter, consisting of large axons encased in large quantities of myelin
sheath. Autistic children as well have been found to have abnormal white
matter in the myelin sheath of the brain, that is also depleted in water content
[15]. Remarkably, some humans are born without a corpus callosum or with
one that is reduced in size, and some of them can function perfectly well in
society. However, a study found that nearly half of children with this defect
had autism traits [16].

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BTBR Mice: Gut Issues

A seminal study on these BTBR mice revealed specific disruptions in the gut
h h h d l d h l l ff h h
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that were hypothesized to lead to the neurological effects through interactions

along the gut–brain axis [18]. The most glaring disorder observed was a
disruption in the synthesis of bile acids in the liver and of their further
modification by gut bacteria. Normally, the liver synthesizes bile acids from
cholesterol and conjugates them with either taurine or glycine before
shipping them out to the gut or buffering them in the gall bladder. It is the
responsibility of specific species of gut bacteria, mainly Bifidobacteria, to
deconjugate the conjugated bile acids, freeing up the taurine or glycine
molecule for further metabolism. This is a necessary step before the bile acids
can be further modified by other gut bacteria, notably the species Blautia,
into secondary bile acids. Thus there are many different variants of the bile
acids, and the distinct forms have differing signaling effects influencing
peristalsis and gut barrier integrity.

These BTBR mice were found to have a deficiency in bile acid synthesis in the
liver, as well as a further deficiency in their deconjugation and their
conversion to secondary bile acids by the microbiota. This was consistent
with an observed notable reduction in the populations of Bifidobacteria and
Blautia.

Did Glyphosate Cause Autism in BTBR Mice?

It is easy to argue that these abnormalities could be due in part to glyphosate

exposure. These mice are the progeny of multiple generations of inbred lab
mice that were almost certainly fed a steady diet of glyphosate in their mouse
feed manufactured from genetically modified Roundup–Ready corn and soy
crops. A reduced supply of bile acids in each generation, and direct toxicity of
glyphosate to certain species of bacteria, would alter the microbial
distribution over time. Thus, the gut microbes that were passed on from
generation to generation could maintain a pathological distribution
influenced by glyphosate acting as an antibiotic and enzyme disruptor [19].

Bile acid synthesis depends crucially on cytochrome P450 (CYP) enzymes in

the liver. Glyphosate has been shown to severely reduce CYP enzyme
expression in the rat liver [19, 20]. A study on poultry microbiota showed that
Bifidobacteria were especially highly sensitive to glyphosate, compared to all
other species examined [21]. It is logical that Bifidobacteria would suffer from
glyphosate exposure due to their role in deconjugating bile acids, because
glyphosate can be expected to substitute for glycine during the conjugation
step, due to the fact that it is an amino acid analogue of glycine [22, 23].
Bifidobacteria would be tasked with deconjugating glyphosate from bile acids,
and then would be directly exposed to the liberated glyphosate molecule
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and then would be directly exposed to the liberated glyphosate molecule.

BTBR mice also exhibited impaired serotonin synthesis which resulted in

slowed peri–stalsis and issues of constipation and small intestinal bacterial
overgrowth (SIBO). This too is easily explained by glyphosate since it
famously disrupts the synthesis of the aromatic amino acids through the
shikimate pathway [19]. The gut microbes produce these essential amino
acids to supply them to the host, and one of them, tryptophan, is the
precursor to serotonin. Furthermore, BTBR mice had reduced levels of acetate
in the gut, a short chain fatty acid normally produced by gut microbes,
especially Bifidobacteria [24], during fat digestion, and an important fuel that
feeds into the Krebs cycle to produce energy. Acetate deficiency in the gut has
also been seen in human autism, and this was linked to a deficiency in
Bifidobacteria [25].

Studies on Mice Exposed to Glyphosate

Exposure of male mice to glyphosate–based herbicides during the juvenile

and adult period led to a marked reduction in serotonin levels in several
nuclei in the brainstem [26]. This was associated with weight loss, decreased
locomotor activity, and an increase in anxiety and depression–like behavior.
Serotonin, whether produced in the brain or the gut, is sulfated in transit, and
melatonin, which is derived from serotonin, is also sulfated. We argued in a
paper published in 2015 that glyphosate could collaborate with aluminum to
induce both gut dysbiosis and disruption of pineal gland function in the brain
[2]. The pineal gland produces sulfated melatonin and distributes it into the
cerebrospinal fluid of the ventricles during sleep. We proposed that an
important role for melatonin is to deliver sulfate to neurons to boost the
sulfate supplies in the HSPGs. Heparan sulfate plays a significant role in the
clearance of cellular debris, which is an important aspect of sleep. And sleep
disturbance is a common feature of autism [27]. So this is getting close to
closing the gap between the heparan sulfate deficiency observed in the brains
of BTBR mice and their gastrointestinal disturbances.

Taurine: Miracle Molecule?

Even before I knew the word glyphosate, I published an article, together with
other colleagues, titled: “Is Encephalopathy a Mechanism to Renew Sulfate in
Autism?” [28]. In this paper, we discussed the crucial role of heparan sulfate
in the brain and a potential link to autism. We proposed that taurine plays a
central role in restoring sulfate supplies to the brain under stressful
conditions. Curiously, human cells are unable to metabolize taurine, but
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y, What We Can Learn from Mouse Models of Autism
,
dietary taurine can get converted to sulfate by gut microbes. The brain, heart
and liver all store large amounts of taurine, and this taurine is released into
circulation during encephalopathy (brain swelling) or during a heart attack.
This taurine is then taken up by the liver and conjugated to bile acids. The
taurine, received by the deconjugating gut microbes, can then be oxidized to
sulfate, to boost supplies in the blood. I suspect, although at this time this is
only speculation, that the bile acids serve a crucial role in facilitating the
reaction that releases the sulfonate moiety from taurine, perhaps by
anchoring the taurine molecule in the bacterial membrane. Further oxidation
by sulfite oxidase yields sulfate. Glyphosate’s damaging effects on
Bifidobacteria would interfere with the production of sulfate from taurine by
gut microbes, due to impairment in the ability to detach taurine from the bile
acids.

Clostridia Overgrowth and Vaccine–Induced Autism

A very different mouse model of autism involves exposure of a pregnant

mouse dam to virus–like particles during gestation. Two publications
describing one such experiment have gained considerable attention from the
media, particularly because they demonstrated a link between a particular
profile of gut microbial colonization in the dam and a susceptibility to autism
in the pups [7, 8]. The pups not only exhibited classic autistic behavior, but
also had “patches of disorganized cortical cytoarchitecture” within a specific
region in the somatosensory cortex of their brains, showing disrupted brain
development architecturally.

The authors noted that the autistic profile only arose if the dam had an over–
representation of a specific filamentous Clostridia strain in the gut, which in
turn led to expression of a “Th17” type immune response by the dam’s
immune system. A communication between the gut and brain led,
remarkably, to a signaling cascade that had a direct impact on the developing
fetuses. The virus–like particles, called “polyinosinic:polycytidylic acid”
(poly(I:C)) were injected into the brain of the dam on embryonic day 12.5.
These particles are not a life form, but they fool the brain’s immune system
into believing that there has been a viral invasion in the brain, and it is the
immune response itself, not the viral infection, that induces the overactive
response adversely affecting brain development in the offspring. And, what is
even more surprising is that the defects develop in the mouse pups only if
there is a particular distribution of gut microbes favoring the filamentous
Clostridia species.

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An earlier study using this same mouse model of injecting a pregnant dam
with poly(I:C) links Clostridia overgrowth to the release of certain specific
toxins, and, remarkably, links these toxins directly to autism [17]. Several
species of Clostridia produce toxic phenolic metabolites such as 4–
ethylphenyl sulfate (4EPS) and p–cresol sulfate. The offspring of exposed
mouse dams displayed a striking 45–fold increase in serum levels of 4EPS, as
well as elevated levels of p–cresol sulfate. This was associated with elevated
levels of inflammatory factors in the maternal blood, placenta and aminiotic
fluid. Notably, a 3–week treatment of young healthy mice with 4EPS
potassium salts was enough to induce autistic symptoms in these mice.
Furthermore, probiotic treatment with the species Bacteroides fragilis
ameliorates autistic symptoms in the offspring of poly(I:C) exposed dams.

These seminal experiments imply that an overgrowth of Clostridia species in

the gut could potentially cause a similar response in a human pregnant
woman receiving a flu vaccine. The study on poultry mentioned earlier
showed a distinct lack of sensitivity to glyphosate among various species of
Clostridia. Glyphosate also induces a leaky gut barrier, likely in part due to
the disruptions of bile acid homeostasis as observed in the study on the BTBR
mice [18], but also through its induction of zonulin synthesis in the
enterocytes of the midgut, directly triggering an opening up of the barrier
[29]. A leaky gut barrier leads to a leaky brain barrier, and this would allow
the vaccine flu virus particles to gain access to the mother’s brain, triggering
an inflammatory response and resulting signaling cascade that altered fetal
development. The disruption in the pups’ brains occurred within the
somatosensory cortex. Intriguingly, the development of nerve fibers in the
corpus callosum connecting the somatosensory cortex between the two
hemispheres depends upon neuronal activity within the somatosensory
cortex, which can be suppressed by certain toxins such as tetanus toxin [30].

Human Studies are Consistent with the Mouse Studies

A recent study by William Shaw involved a set of triplets, two boys and a girl
[31]. Both boys were diagnosed with autism and the girl had a seizure
disorder. All three children were found to have high levels of glyphosate in
their urine. They also had overrepresentation of Clostridia species in the gut,
which were suggested to contribute to the disease process through their
release of toxic phenolic metabolites. Another study from 2017 on the gut
microbiome of autistic children with inflammatory bowel disease compared
to normal controls showed reduced Blautia species (impaired bile acid
metabolism) and increases in several species of Clostridia that were linked to
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reduced tryptophan levels and impaired serotonin homoestasis, along with

overexpression of Th17, all consistent with the various mouse model studies
[32].

Conclusion

In summary, a disrupted gut microbiome (which can be caused by

glyphosate) leads to a leaky gut barrier, a leaky brain barrier and a leaky
placental barrier. This allows toxic substances such as aluminum, phenolic
compounds and glyphosate, as well as live viruses and endotoxins from
vaccines, to invade the brain, and, by breaching the placental barrier, expose
the fetus to harm. An overzealous immune reaction to these insults disrupts
neuronal development and causes autistic–like behaviors in the mouse pups
and in children whose mothers have been similarly exposed.

The BTBR mice became autistic after many generations of inbreeding during
glyphosate exposure in the lab. It would be very interesting to find out what
would happen if a group of BTBR mice were provided a nutrient–dense
organic diet and clean water, and allowed to reproduce through multiple
generations with this healthy diet. Would the descendants eventually lose
their autism diagnosis? If they did, it would tell us a great deal about the
importance of an organic diet to human health, and would greatly strengthen
the idea that glyphosate is a causative factor in autism

Republished from GreenMedInfo.com

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Stephanie Seneff Follow

Stephanie Seneff is a Senior Research Scientist at the MIT

Computer Science and Artificial Intelligence Laboratory. She
received the B.S. degree in Biophysics in 1968, the M.S. and
E.E. degrees in Electrical Engineering in 1980, and the Ph.D
degree in Electrical Engineering and Computer Science in
1985, all from MIT. For over three decades, her research
interests have always been at the intersection of biology and
computation: developing a computational model for the
human auditory system, understanding human language so
as to develop algorithms and systems for human computer
interactions, as well as applying natural language processing
(NLP) techniques to gene predictions. She has published over
170 refereed articles on these subjects, and has been invited
to give keynote speeches at several international conferences.
She has also supervised numerous Master’s and PhD theses
at MIT. In 2012, Dr. Seneff was elected Fellow of the
International Speech and Communication Association
(ISCA).

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