AUTISM and VACCINS - 6 (English)
Relazione-Dossier del dott. M. Montinari su Autismo dai Vaccini
PROTOCOLLO DAN (dott. F. Verzella)
AUTISMO dai VACCINI - SENTENZA del TRIBUNALE
vedi qui: il PDF dello studio che indica la correlazione fra Autismo e Vaccini
INTERVISTA con il dott. William Shaw (USA)
Metalli tossici dei vaccini = Autismo vedi: PDF -  (dott. M. Proietti)
Sindrome della permeabilita' intestinale ed autismo
Il Thimerosal dei vaccini distrugge e/o altera la flora intestinale essendo una sostanza altamente tossica
MINERALOGRAMMA (test per conoscere il livello ed il tipo di intossicazioni da minerali e metalli tossici anche dei vaccini)
Il Thiomersal dei vaccini produce danni anche gravi
Metalli tossici
Danni al sistema enzimatico da Vaccini e metalli 
By Giusy Arcidiacono (CT) - arcidiaconogiusy@hotmail.com - Perito Commerciale - chimico
Ecco il recente studio che ha coinvolto più di 17.000 bambini fino a 19 anni
Questo studio-indagine attualmente in corso è stato avviato dall’omeopata Andreas Bachmair.
La Verita' sullo studio del dott. Wakefield
Terapia Naturale per l'Autismo (Gaps)
AUTISMO e malattie varie dai Vaccini - Studi Pubblicati - PDF
 

Vaccinazioni per l’infanzia ed autismo
Metalli tossici dei vaccini = Autismo vedi: PDF -  dott. M. Proietti

Sentenza 2012 - Trib. Rimini su Vaccini=Autismo

II.       COMPARISON OF BIOLOGICAL ABNORMALITIES
Like the similarities seen in observable symptoms, parallels between autism and mercury poisoning clearly exist even at cellular and subcellular levels. These similarities are summarized in tables after each individual section.

a.      Biochemistry

Sulfur:  Studies of autistic children with known chemical or food intolerances show a low capacity to oxidize sulfur compounds and low levels of sulfate (O’Reilly & Waring, 1993; Alberti et al, 1999).  These findings were interpreted as suggesting that “there may be a fault either in the manufacture of sulfate or that sulfate is being used up dramatically on an unknown toxic substance these children may be producing” (O'Reilly and Waring, 1993).  Alternatively, these observations may be linked to mercury, since mercury preferentially forms compounds with molecules rich in sulfhydryl groups (--SH), such as cysteine and glutathione,making them unavailable for normal cellular and enzymatic functions (Clarkson, 1992). Relatedly, mercury may cause low sulfate by its ability to irreversibly inhibit the sulfate transporter Na-Si cotransporter NaSi-1 present in kidneys and intestines, thus preventing sulfate absorption (Markovitch and Knight, 1998).
Among the sulfhydryl groups, or thiols, mercury has special affinity for purines and pyrimidines, as well as other subcellular substances (Clarkson, 1992; Koos and Longo, 1976).  Errors in purine or pyrimidine metabolism are known to result in classical autism or autistic features in some cases (Gillberg and Coleman, 1992, p.209; Page et al, 1997; Page & Coleman, 2000; The Purine Research Society), thereby suggesting that mercury’s disruption of this pathway might also lead to autistic traits.
Likewise, yeast strains sensitive to Hg are those which have innately low levels of tyrosine synthesis. 
Mercury can deplete cellular tyrosine by binding to the SH-groups of the tyrosine uptake system, preventing colony growth (Ono et al, 1987), and Hg-depleted tyrosine would be particularly significant in cells known to accumulate mercury (e.g., neurons of the CNS, see below).  Similarly, disruptions in tyrosine production in hepatic cells, arising from a genetic condition called Phenylketonuria (PKU), also results in autism (Gillberg & Coleman, 1992, p.203).
Glutathione:  Glutathione is one of the primary meansthrough which the cells detoxify heavy metals (Fuchs et al, 1997), and glutathione in the liver is a primary substrate by which body clearance of organic mercury takes place (Clarkson, 1992).  Mercury, by preferentially binding with glutathione and/or preventing absorption of sulfate, reduces glutathione bioavailability.  Many autistic subjects have low levels of glutathione.  O’Reilly and Waring (1993) suggest this is due to an “exotoxin” binding glutathione so it is unavailable for normal biological processes.  Edelson and Cantor (1998) have found a decreased ability of the liver in autistic subjects to detoxify heavy metals.  Alternatively, low glutathione can be a manifestation of chronic infection (Aukrust et al, 1996, 1995; Jaffe et al, 1993), and infection-induced glutathione deficiency would be more likely in the presence of immune impairments derived from mercury (Shenkar et al, 1998).
Glutathione peroxidase activities were reported to be abnormal in the erythrocytes of autistic children (Golse et al, 1978).  Mercury generates reactive oxygen species (ROS) levels in cells, which increases ROS scavenger enzyme content and thus glutathione, to relieve oxidative stress (Hussain et al, 1999). 
At high enough levels, mercury depletes rat hepatocytes of glutathione (GSH) and causes significant reduction in glutathione peroxidase and glutathione reductase (Ashour et al, 1993).
Mitochondria:  Disturbances of brain energy metabolism have prompted autism to be hypothesized as a mitochondrial disorder (Lombard, 1998).  There is a frequent association of lactic acidosis and carnitine deficiency in autistic patients, which suggests excessive nitric oxide production in mitochondria (Lombard, 1998; Chugani et al, 1999), and again, mercury may be a participant.  Methylmercury accumulates in mitochondria, where it inhibits several mitochondrial enzymes, reduces ATP production and Ca2+ buffering capacity, and disrupts mitochondrial respiration and oxidative phosphorylation (Atchison & Hare, 1994; Rajanna and Hobson, 1985; Faro et al, 1998).  Neurons have increased numbers of mitochondria (Fuchs et al, 1997), and since Hg accumulates in neurons of the CNS, an Hg effect upon neuronal mitochondria function seems likely - especially in children having substandard mercury detoxification.

b.   Immune System

A variety of immune alterations are found in autism-spectrum children (Singh et al, 1993;Gupta et al, 1996; Warren et al, 1986 & 1996; Plioplys et al, 1994), and these appear to be etiologically significant in a variety of ways, ranging from autoimmunity to infections and vaccination responses (e.g., Fudenberg, 1996; Stubbs, 1976).  Mercury’s effects upon immune cell function are well documented and may be due in part to the ability of Hg to reduce the bioavailability of sulfur compounds:
“It has been known for a long time that thiols are required for optimal primary in vitro antibody response, cytotoxicity, and proliferative response to T-cell mitogens of murine lymphoid cell cultures.  Glutathione and cysteine are essential components of lymphocyte activation, and their depletion may result in lymphocyte dysfunction.  Decreasing glutathionelevels profoundly affects early signal transduction events in human T-cells” (Fuchs & Schöfer, 1997).
Allergy, asthma, and arthritis:  Individuals with autism are more likely to have allergies and asthma, and autism occurs at a higher than expected rate in families with a history of autoimmune diseases such as rheumatoid arthritis and hypothyroidism (Comi and Zimmerman, 1999; Whitely et al, 1998).  Relative to the general population, prevalence of selective IgA deficiency has been found in autism (Warren et al); individuals with selective IgA deficiency are more prone to allergies and autoimmunity (Gupta et al, 1996).  Furthermore, lymphocyte subsets of autistic subjects show enhanced expression of HLA-DR antigens and an absence of interleuken-2 receptors,and these findings are associated with autoimmune diseases like rheumatoid arthritis (Warren et al).  These observations suggest autoimmune processes are present in ASD (Plioplys, 1989; Warren et al); and this possibility is reinforced by Singh’s findings of elevated antibodies against myelin-basic protein (Singh et al, 1993).
Atypical responses to mercury have been ascribed to allergic or autoimmune reactions (Gosselin et al, 1984; Fournier et al, 1988), and genetic predisposition for Hg reaction may explain why sensitivity to this metal varies so widely by individual (Rohyans et al, 1984; Nielsen & Hultman, 1999).  Acrodynia can present as a hypersensitivity reaction (Pfab et al, 1996), or it may arise from immune over-reactivity, and “children who incline to allergic reactions have an increased tendency to develop acrodynia” (Warkany & Hubbard, 1953).  Those with acrodynia are also more likely to suffer from asthma, to have poor immune system function (Farnesworth, 1997), and to experience intense joint pains suggestive of rheumatism (Clarkson, 1997).  Methylmercury has altered thyroid function in rats (Kabuto, 1991).
Rheumatoid arthritis with joint pain has been observed as a familial trait in autism (Zimmerman et al, 1993). 
A subset of autistic subjects had a higher rate of strep throat and elevated levels of B lymphocyte antigen D8/17, which has expanded expression in rheumatic fever and may be implicated in obsessive-compulsive behaviors (DelGiudice-Asch & Hollander, 1997).
Mercury exposure frequently results in rheumatoid-like symptoms.  Iraqi mothers and children developed muscle and joint pain (Amin-Zaki, 1979), and acrodynia is marked by joint pain (Farnesworth, 1997).  Sore throat is occasionally a presenting sign in mercury poisoning (Vroom and Greer, 1972). A 12 year old with mercury vapor poisoning, for example, had joint pains as well as a sore throat; she was positive on a streptozyme test, and a diagnosis of rheumatic fever was made; she improved on penicillin (Fagala and Wigg, 1992).  Acrodynia, which is almost never seen in adults, was also observed in a 20 year old male with a history of sensitivity reactions and rheumatoid-like arthritis, who received ethylmercury via injection in gammaglobulin (Matheson et al, 1980). 
One effective chelating agent, penicillamine, is also effective for rheumatoid arthritis (Florentine and Sanfilippo, 1991).
Mercury can induce an autoimmune response in mice and rats, and the response is both dose-dependent and genetically determined.  Mice “genetically prone to develop spontaneous autoimmune diseases [are] highly susceptible to mercury-induced immunopathological alterations” (al-Balaghi, 1996). 
The autoimmune response depends on the H-2 haplotype:  if the strain of mice does not have the susceptibility haplotype, there is no autoimmune response; the most sensitive strains show elevated antibody titres at the lowest dose; and the less susceptible strain responds only at a medium dose (Nielsen & Hultman, 1999).  Interestingly, Hu et al (1997) were able to induce a high proliferative response in lymphocytes from even low responder mouse strains by washing away excess mercury after pre-treatment, while chronic exposure to mercury induced a response only in high-responder strains.
Autoimmunity and neuronal proteins:  Based upon research and clinical findings, Singh has been suggesting for some time an autoimmune component in autism (Singh, Fudenberg et al, 1988).  The presence of elevated serum IgG “may suggest the presence of persistent antigenic stimulation” (Gupta et al, 1996).  Connolly and colleagues (1999) report higher rates in autistic vs. control groups of elevated antinuclear antibody (ANA) titers, as well as presence of IgG and IgM antibodies to brain endothelial cells.
On the one hand,since mercury remains in the brain for years after exposure, autism’s persistent symptoms may be due to an on-going autoimmune response to mercury remaining in the brain; on the other hand, activation and continuation of an autoimmune response does not require the continuous presence of mercury ions: in fact, once induced, autoimmune processes in the CNS might remain exacerbated because removal of mercury after an initial exposure can induce a greater proliferative response in lymphocytes than can persistent Hg exposure (Hu et al, 1997).
In sera of male workers exposed to mercury, autoantibodies (primarily IgG) to neuronal cytoskeletal proteins, neurofilaments (NFs), and myelin basic protein (MBP) were prevalent.  These findings were confirmed in rats and mice, and there were significant correlations between IgG titers and subclinical deficits in sensorimotor function.  These findings suggest that peripheral autoantibodies to neuronal proteins are predictive of neurotoxicity, since histopathological findings were associated with CNS and PNS damage.  There was also evidence of astrogliosis (indicative of neuronal CNS damage) and the presence of IgG concentrated along the bbb (El-Fawal et al, 1999).  Autoimmune response to mercury has also been shown by the transient presence of antinuclear antibodies (ANA) and antinucleolar antibodies (ANolA) (Nielsen & Hultman, 1999; Hu et al, 1997; Fagala and Wigg, 1992).
A high incidence of anti-cerebellar immunoreactivity which was both IgG and IgM in nature has been found in autism, and there is a higher frequency of circulating antibodies directed against neuronal antigens in autism as compared to controls (Plioplys, 1989; Connolly et al, 1999).  Furthermore, Singh and colleagues have found that 50% to 60% of autistic subjects tested positive for the myelin basic protein antibodies (1993) and have hypothesized that autoimmune responses are related to an increase in select cytokines and to elevated serotonin levels in the blood (Singh, 1996; Singh, 1997).  Weitzman et al(1982) have also found evidence of reactivity to MBP in autistic subjects but none in controls.
Since anti-cerebellar antibodies have been detected in autistic blood samples, ongoing damage may arise as these antibodies find and react with neural antigens, thus creating autoimmune processes possibly producing symptoms such as ataxia and tremor.  Relatedly, the cellular damage to Purkinje and granule cells noted in autism (see below) may be mediated or exacerbated by antibodies formed in response to neuronal injury (Zimmerman et al, 1993).
T-cells, monocytes, and natural killer cells:  Many autistics have skewed immune-cell subsets and abnormal T-cell function, including decreased responses to T-cell mitogins (Warren et al, 1986; Gupta et al, 1996).  One recent study reported increased neopterin levels in urine of autistic children, indicating activation of the cellular immune system (Messahel et al, 1998).
Workers exposed to Hgo exhibit diminished capacity to produce the cytokines TNF (alpha) and IL-1 released by monocytes and macrophages (Shenkar et al, 1998).  Both high dose and chronic low-level mercury exposure kills lymphocytes, T-cells, and monocytes in humans.  This occurs by apoptosis due to perturbation of mitochondrial dysfunction.  At low, chronic doses, the depressed immune function may appear asymptomatic, without overt signs of immunotoxicity.  Methylmercury exposure would be especially harmful in individuals with already suppressed immune systems (Shenker et al, 1998).  Mercury increases cytosolic free calcium levels [Ca2+]i in T lymphocytes, and can cause membrane damage at longer incubation times (Tan et al, 1993). 
Hg has also been found to cause chromosomal aberrations in human lymphocytes, even at concentrations below those causing overt poisoning (Shenkar et al, 1998; Joselow et al, 1972), and to inhibit rodent lymphocyte proliferation and function in vitro.
Depending on genetic predisposition, mercury causes activation of the immune system, especially Th2 subsets, in susceptible mouse strains (Johansson et al, 1998; Bagenstose et al, 1999; Hu et al, 1999).  Many autistic children have an immune portrait shifted in the Th2 direction and have abnormal CD4/CD8 ratios (Gupta et al, 1998; Plioplys, 1989).  This may contribute to the fact that many ASD children have persistent or recurrent fungal infections (Romani, 1999).
Many autistic children have reduced natural killer cell function (Warren et al, 1987; Gupta etal, 1996), and many have a sulfation deficiency (Alberti, 1999).  Mercury reduces --SH group/sulfate availability, and this has immunological ramifications.  As noted previously, decreased levels of glutathione, observed in autistic and mercury poisoned populations, are associated with impaired immunity (Aukrust et al, 1995 and 1996;
Fuchs and Schöfer, 1997).  Decreases in NK T-cell activity have in fact been detected in animals after methylmercury exposure (Ilback, 1991).
Singh detected elevated IL-12 and IFNg in the plasma of autistic subjects (1996). Chronic mercury exposure induces IFNg and IL-2 production in mice, while intermittent presence of mercury suppresses IFNg and enhances IL-4 production (Hu et al, 1997).  Interferon gamma (IFNg) is crucial to many immune processes and is released by T lymphocytes and NK cells, for example, in response to chemical mitogens and infection;  sulfate participates in IFNg release, and “the effector phase of cytotoxic T-cell response and IL-2-dependent functions is inhibited by even a partial depletion of the intracellular glutathione pool” (Fuchs & Schöfer, 1997).  A mercury-induced sulfation problem might, therefore, impair responses to viral (and other) infections - via disrupting cell-mediated immunity as well asby impairing NK function (Benito et al, 1998).  In animals, Hg exposure has led to decreases in production of antibody-producing cells and in antibody titres in response to inoculation with immune-stimulating agents (EPA, 1997, review, p.3-84).
 

c.   CNS Structure
Autism is primarily a neurological disorder (Minshew, 1996), and mercury preferentially targets nerve cells and nerve fibers (Koos and Longo, 1976).  Experimentally, primates have the highest levels in the brain relative to other organs (Clarkson, 1992).  Methylmercury easily crosses the blood-brain barrier by binding with cysteine to form a molecule that is nearly identical to methionine.  This molecule - methylmercury cysteine - is transported on the Large Neutral Amino Acid across the bbb (Clarkson, 1992).
Once in the CNS, organic mercury is converted to the inorganic form (Vahter et al, 1994).  Inorganic mercury is unable to cross back out of the bbb (Pedersen et al, 1999) and is more likely than the organic form to induce an autoimmune response (Hultman and Hansson-Georgiadis, 1999).  Furthermore, although most cells respond to mercurial injury by modulating levels of glutathione, metallothionein, hemoxygenase, and other stress proteins, “with few exceptions, neurons appear to be markedly deficient in these responses” and thus more prone to injury and less able to remove the metal (Sarafian et al, 1996).
While damage has been observed in a number of brain areas in autism, many functions are spared (Dawson, 1996).  In mercury exposure, damage is also selective (Ikeda et al, 1999; Clarkson, 1992), and the list of Hg-affected areas is remarkably similar to the neuroanatomy of autism.
Cerebellum, Cerebral Cortex, & Brainstem: Autopsy studies of carefully selected autistic individuals revealed cellular changes in cerebellar Purkinje and granule cells (Bauman and Kemper, 1988; Ritvo  et al, 1986).  MRI studies by Courchesne and colleagues (1988; reviewed in ARI Newslett, 1994) described cerebellar defects in autistic subjects, including smaller vermal lobules VI and VII and volume loss in the parietal lobes. 
The defects werepresent independently of IQ.  “No other part of the nervous system has been shown to be so consistently abnormal in autism.”  Courchesne (1989) notes that the only neurobiological abnormality known to precede the onset of autistic symptomatology is Purkinje neuron loss in the cerebellum. 
Piven found abnormalities in the cerebral cortex in seven of 13 high-functioning autistic adults using MRI (1990).  Although more recent studies have called attention to amygdaloid and temporal lobe irregularities in autism (see below), and cerebellar defects have not been found in all ASD subjects studied (Bailey et al, 1996), the fact remains that many and perhaps most autistic children have structural irregularities within the cerebellum.
Mercury can induce cellular degeneration within the cerebral cortex and leads to similar processes within granule and Purkinje cells of the cerebellum (Koos and Longo, 1976; Faro et al, 1998; Clarkson, 1992; see also Anuradha, 1998; Magos et al, 1985). Furthermore, cerebellar damage isimplicated in alterations of coordination, balance, tremors, and sensations (Davis et al, 1994; Tokuomi et al, 1982), and these findings are consistent with Hg-induced disruption in cerebellar synaptic transmission between parallel fibers or climbing fibers and Purkinje cells (Yuan & Atchison, 1999).
MRI studies have documented Hg-effects within visual and sensory cortices, and these findings too are consistent with the observed sensory impairments in victims of mercury poisoning (Clarkson, 1992; Tokuomi et al, 1982).  Acrodynia, a syndrome with symptoms similar to autistic traits, is considered a pathology mainly of the CNS arising from degeneration of the cerebral and cerebellar cortex (Matheson et al, 1980). In monkeys, mercury preferentially accumulated in the deepest pyramidal cells and fiber systems.
Mercury causes oxidative stress in neurons.  The CNS cells primarily affected are those which are unable to produce high levels of protective metallothionein and glutathione.  These substances tend to inhibit lipid peroxidation and thereby suppress mercury toxicity (Fukino et al, 1984).  Importantly, granule and Purkinje cells have increased risk for mercury toxicity because they produce low levels of these protective substances (Ikeda et al, 1999; Li et al, 1996).  Naturally low production of glutathione, when combined with mercury’s ability to deplete usable glutathione reserves, provides a mechanism whereby mercury is difficult to clear from the cerebellum -- and this is all the more significant because glutathione is a primary detoxicant in brain (Fuchs et al, 1997).
Mercury’s induction of cerebellar deterioration is not restricted to high-doses.  Micromolar doses of methylmercury cause apoptosis of developing cerebellar granule cells by antagonizing insulin-like growth factor (IGF-I) and increasing expression of the transcription factor c-Jun (Bulleit and Cui, 1998).
Several researchers have found evidence of a brainstem defect in a subset of autistic subjects (Hashimoto et al, 1992 and 1995; McClelland et al, 1985); and MRI studies have revealed brainstem damage in a few cases of mercury poisoning (Davis et al, 1994).  The peripheral polyneuropathy examined in Iraqi victims was believed to have resulted from brain stem damage (Von Burg and Rustam, 1974).
Amygdala & Hippocampus: Atypicalities in other brain areas are remarkably similar in ASD and mercury poisoning.  Pathology affecting the temporal lobe, particularly the amygdala, hippocampus, and connected areas, is seen in autistic patients and is characterized by increased cell density and reduced neuronal size (Abell et al, 1999; Hoon and Riess, 1992; Otsuka, 1999; Kates et al, 1998; Bauman and Kemper, 1985). 
The basal ganglia also show lesions in some cases (Sears, 1999), including decreased bloodflow (Ryu et al, 1999).
Mercury can accumulate in the hippocampus and amygdala, as well as the striatum and spinal chord (Faro et al, 1998; Lorscheider et al, 1995; Larkfors et al, 1991).  One study has shown that areas of hippocampal damage from Hg were those which were unable to synthesize glutathione (Li et al, 1996). 
A 1994 study in primates found that mercury accumulates in the hippocampus and amygdala, particularly the pyramidal cells, of adults and offspring exposed prenatally (Warfvinge et al, 1994).
The documenting of temporal lobe mercury provides a direct link between autism and mercury because, as cited previously, (i) mercury alters neuronal function, and (ii) the temporal lobe, and the amygdala in particular, are strongly implicated in autism (e.g., Aylward et al, 1999; Bachevalier, 1994; Baron-Cohen, 1999; Bauman & Kemper, 1985; Kates et al, 1998; Nowell et al, 1990; Warfvinge et al, 1994).  Bachevalier (1996) has shown that infant monkeys with early damage to the amygdaloid complex exhibitmany autistic behaviors, including social avoidance, blank expression, lack of eye contact and play posturing, and motor stereotypies. 
Hippocampal lesions, when combined with amygdaloid damage, increases the severity of symptoms.
Also noteworthy is the fact that amygdala findings in autism and mercury literatures are paralleled in fragile X syndrome, a genetic disorder wherein many affected individuals have traits worthy of an autism diagnosis.  These traits include sensory alterations, emotional lability, appetite dysregulation, social deficits, and eye-contact aversion (Hagerman).  Not only are fraX-related proteins (FRM1, FMR2) implicated in amygdaloid function (Binstock, 1995; Yamagata, 1999), but neurons involved in gaze- and eye-contact-aversion havebeen identified within the primate temporal lobe and amygdaloid subareas (Rolls 1992, reviewed in Binstock 1995).  These various findings in ASD, mercury poisoning, and fragile X suggest that amygdaloid mercury is a mechanism for inducing traits central to or associated with autism and the autism-spectrum of disorders.
Neuronal Organization & Head Circumference: Several autism brain studies have found evidence of increased neuronal cell replication, a lowered ratio of glia to neurons, and an increased number of glial cells (Bailey et al, 1996).  Based on these and other neuropathological findings, autism can be characterized as “a disorder of neuronal organization, that is, the development of the dendritic tree, synaptogenesis, and the development of the complex connectivity within and between brain regions” (Minshew, 1996).
Mercury can interfere with neuronal migration and depress cell division in the developing brain. 
Post-mortem brain tissue studies of exposed Japanese and Iraqi infants revealed “abnormal neuronal cytoarchitecture characterized by ectopic cells and disorganization of cellular layers” (EPA, 1997, p.3-86; Clarkson, 1997). Developmental neurtoxicity of Hg may also be due to binding of mercury to sulfhydryl-rich tubulin, a component of microtubules (Pendergrass et al, 1997).  Intact microtubules are necessary for proper cell migration and cell division (EPA, review, 1997, p.32-88).
Rat pups dosed postnatally with methylmercury had significant reductions in neuralcell adhesion molecules (NCAMs), which are critical during neurodevelopment for proper synaptic structuring. 
Sensitivity of NCAMs to methylmercury decreased as the developmental age of the rats increased.  “Toxic perturbation of the developmentally-regulated expression of NCAMs during brain formation may disturb the stereotypic formation of neuronal contacts and could contribute to the behavioral and morphological disturbances observed following methylmercury poisoning" (Deyab et al, 1999).  Plioplys et al (1990) have found depressed expression of NCAM serum fragments in autism.
Abnormalities in neuronal growth during development are implicated in head size differences found in both autism and mercury poisoning.  In autism, Fombonne and colleagues (1999) have found a subset of subjects with macrocephaly and a subset with microcephaly.  The circumference abnormalities were progressive, so that, while micro- and macrocephaly were present in 6% and 9% respectively of children under 5 years, among those age10-16 years, the rates had increased to 39% and 24% respectively. 
Another study, by Stevenson et al (1997), had found just one subject out of 18 with macrocephaly who had this abnormality present at birth.  The macrocephaly in autism is generally believed to result from “increased neuronal growth or decreased neuronal pruning.”  The cause of microcephaly has not been investigated.
The most detailed study of head size in mercury poisoning, by Amin-Zaki et al (1979), involved 32 Iraqi children exposed prenatally and followed up to age 5 years.  Eight (25%) had progressive microcephaly, i.e., the condition was not present at birth.  None had developed macrocephaly, at least at the time of the study. 
The microcephaly has been ascribed to neuronal death or apoptosis from Hg intoxication.

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