Vijendra K. Singh, Ph.D. : Selected Research on
Autism Research Associate Professor, Utah State University Dept. of Biology/Biotechnology Center Scientific Board Member, Autism Autoimmunity Project
Dr. V. K. Singh received his doctorate from the
University of British Columbia, Vancouver, Canada. His post-doctoral
fellowship was completed in neurochemistry and neuroimmunology. Spanning
over twenty years' experience in neurobiology and immunology research, Dr.
Singh studied brain diseases, particularly infantile autism and Alzheimer's
disease. Having authored over a hundred scientific publications, he is both
a pioneer and an international authority on autoimmunity in autism. Dr.
Singh is a member of the American Association for the Advancement of
Sciences, the American Association of Immunologists, and the New York
Academy of Sciences. He is listed in American Men and Women in Science
(United States, R. R. Bowker, publisher) and The International Who's Who
of Intellectuals (Cambridge, England, International Biographical
V. K. Singh's "Immunotherapy for Brain Diseases and Mental Illnesses"
(Progress in Drug Research), vol. 48, 1997, pp. 129-146) is a lengthy
scientific article addressing the rationale for immunotherapy in brain diseases
and possible applications of specific immunological therapies in Multiple
sclerosis; Guillain-Barre syndrome; Rasmussen's encephalitis;
Obsessive-compulsive disorder (OCD); Alzheimer's disease; and Autistic
syndrome. The introduction to this article notes the growing comprehension
among scientists of the reciprocal relationship between the nervous and immune
systems, categorizes the various diseases of the nervous system, and observes
that nearly all central nervous system diseases respond to immunotherapy.
Selected Research on Autism
"Serological Detection of Measles Virus in Relation to Autoimmunity in
Autism," 102nd General Meeting of the American Society for Microbiology,
May 19-23, 2002, Salt Lake City, Utah, Presentation V-5. Autoimmunity to brain
myelin protein (MBP) secondary to a measles infection may cause autistic
regression in some children with this neurodevelopmental disorder. ...there is a
strong correlation between MMR antibodies and MBP autoantibodies in autism. By
using monoclonal antibodies, we characterized that the MMR antibodies are due to
the measles subunit, but not due to mumps or rubella subunits, of the polyvalent
vaccine. In light of the new evidence presented here, we suggest that the MMR
vaccine in some cases of autism might cause autoimmunity and it might do so by
bringing on an atypical measles infection that does not produce a typical
measles rash but manifests neurological symptoms upon immunization. It is
confirmed here (in an additional population) that this antibody is not typically
produced during normal immune response to the vaccine.
"Abnormal Measles Serology and Autoimmunity in Autistic Children,"
Journal of Allergy and Clinical Immunology, vol. 109, no. 1, S232, January
2002 (abstract #702). Immunoblotting analysis in recent work showed the
presence of an unusual MMR antibody in 60% (75 of 125) of autistic children, but
in none of 92 normal children. By using MMR blots and monoclonal antibodies, we
found that the specific increase of MV antibodies or MMR antibodies was related
to measles hemagglutinin antigen (MV-HA), but not to the mumps or rubella viral
proteins within the MMR vaccine. In addition, over 90% of MMR antibody-positive
autistic sera were also positive for MBP autoantibodies, suggesting a causal
association between MMR and brain autoimmunity in autism. Stemming from this
evidence, we suggest that an "atypical" measles infection in the absence of a
rash but with neurological symptoms might be etiologically linked to
autoimmunity in autism.
"Serological Association of Measles Virus and Human Herpesvirus-6 With
Brain Autoantibodies in Autism." Clinical Immunology and Immunopathology,
vol. 89, number 1, October 1998, pp. 105-8. This study is the first to report an
association between virus serology and brain autoantibody in autism; it supports
the hypothesis that a virus-induced autoimmune response may play a causal role
"Positive Titers of Measles and Measles-Mumps-Rubella Antibody Are Related
to Myelin Basic Protein Autoantibody in Autism." Abstract of study prepared
for the annual meeting of the American Association of Immunologists (AAI) /
Federation of American Societies for Experimental Biology (FASEB), San
Francisco, April 1998. A significant number of autistic children exhibit
positive titers of measles and MMR [measles-mumps-rubella] antibody, which in a
vast majority of cases is associated with the presence of MBP [myelin basic
protein, or brain] autoantibody. A measles- and/or MMR-triggered autoimmune
response to myelin may play a pathogenesis role in autism.
Association of Anti-MBP and Anti-NAFP Antibodies With HHV-6 Antibodies in
a Child With Autistic Regression. Journal of Allergy and Clinical
Immunology, vol. 101, no. 1, part 2, S122, January 1998 (in section
entitled, Program and Abstracts of Papers to Be Presented During Scientific
Sessions [at the] 54th Annual Meeting, March 13-18, 1998). Children with
autism have been shown to have a high incidence of circulating autoantibodies to
myelin basic protein (MBP) and to neuron-axon filament protein (NAFP) compared
with healthy controls or controls with other disabilities. Subacute viral
infections of the central nervous system have been postulated to play a role in
children who develop normally before undergoing autistic regression. In this
instance, a healthy boy having a typical case of roseola (HHV-6) at 15 months
experienced severe regressions of language and social behavior soon afterward.
The presence of antibodies against MBP and NAFP along with the clinical course
and elevated levels of HHV-6 antibodies suggest an autoimmune response to this
neurotropic virus[,] resulting in the autistic regression.
"Circulating Autoantibodies to Neuronal and Glial Filament Proteins in
Autism." Pediatric Neurology, vol. 17, number 1, July 1997, pp.
88-90. A significant increase in incidence of anti-NAFP
[neuron-axon-filament-protein] and anti-GFAP was seen in autistic subjects, but
not in mentally retarded subjects. Clinically, these autoantibodies may be
related to autoimmune pathology in autism.
"Hyperserotoninemia and Serotonin Receptor Antibodies in Children With
Autism but Not Mental Retardation." Biological Psychiatry, vol. 41,
number 6, March 15, 1997, pp. 753-5.
"Elevated Serotonin Levels in Autism: Association With the Major
Histocompatibility Complex." Neuropsychobiology, vol. 34, number 2,
1996, pp. 72-5. Two of the most consistently observed biological findings in
autism are increased serotonin levels in the blood and immunological
abnormalities (including autoreactivity with tissues of the central nervous
system). The major histocompatibility complex (MHC) regulates the immune system,
and is associated with autoimmune disorders. In this study, a positive
relationship was observed between elevated serotonin levels and the MHC types
previously associated with autism.
"Plasma Increase of Interleukin-12 and Interferon-gamma. Pathological
Significance in Autism." Journal of Neuroimmunology, vol. 66, numbers
1-2, May 1996, pp. 143-5. Immune factors such as autoimmunity have been
implicated in the genesis of autism, a neurodevelopmental disorder. Since
autoimmune response involves immune activation, the plasma levels of
interferon-alpha (IFN-alpha), IFN-gamma, interleukin-12 (IL-12), and IL-6 were
measured, along with tumor necrosis factor (TNF-alpha) and soluble intercellular
adhesion molecule-1 (sICAM-1). The levels of IL-12 and IFN-gamma were
significantly higher in autistic patients than in controls (the remaining
measures were not significantly different). It is suggested that IL-12 and IFN-gamma
increases may indicate antigenic stimulation of Th-1 cells pathogenetically
linked to autoimmunity in autism.
"Immunogenetic Studies in Autism and Related Disorders." Molecular
Chemistry and Neuropathology, vol. 28, numbers 1-3, May-August 1996, pp.
77-81. The major histocompatibiligy complex comprises a number of genes that
control the function and regulation of the immune system. One of these, the C4B
gene, encodes a product that is involved in eliminating pathogens such as
viruses and bacteria from the body. A deficient form of the C4B gene, termed the
C4B null allele (no C4B protein produced) was previously seen to have an
increased frequency in autism. In this study, this finding was confirmed, and
this same condition was detected in related [neurodevelopmental] disorders as
well. In addition, two alleles of the DR beta 1 gene also had significantly
increased representation in autistic subjects.
"Antibodies to Myelin Basic Protein in Children With Autistic Behavior."
Brain, Behavior and Immunity, vol. 7, number 1, March 1993, pp. 97-103.
Approximately 58% of the sera of autistic children were found to be positive for
anti-MBP [anti-brain antibodies]. This result was significantly different from
that of the controls, among whom were children with normal health, idiopathic
mental retardation, and Down syndrome. It is possible that anti-MBP antibodies
are associated with the development of autistic behavior.
"Possible Association of the Extended MHC Haplotype B44-SC30-DR4 With
Autism." Immunogenetics, vol. 36, number 4, 1992, pp. 203-7. The
complement C4B null allele appears to be associated with infantile autism. In
this study, the incidence of B44-SC30-DR4 was increased by almost six-fold in
the autistic subjects as compared with healthy controls. Moreover, the total
number of extended haplotypes expressed on chromosomes of autistic subjects was
significantly increased as compared with those expressed on chromosomes of
healthy subjects. Conclusion: a gene related to, or included in, the extended
major histocompatibility complex may be associated with autism.
"Increased Frequency of the Null Allele at the Complement C4b Locus in
Autism." Clinical Experiments in Immunology, vol. 83, number 3, March
1991, pp. 438-40. Associations between C4 deficiency and autoimmune disorders
have been found over the past several years. In this study, autistic subjects
and their mothers had significantly increased phenotypic frequencies of the C4B
null allele, compared with controls. The siblings of the autistic subjects also
had an increased frequency of the C4B null allele, but this was not significant.
The fathers did not display this allele. All family members had normal
frequencies of the C4A null allele, all normal C4A and C4B alleles and all BF
and C2 alleles.
"Changes of Soluble Interleukin-2, Interleukin-2 Receptor, T8 Antigen, and
Interleukin-1 in the Serum of Autistic Children." Clinical Immunology and
Immunopathology, vol. 61, number 3, December 1991, pp. 448-455. Findings
indirectly indicated that the activation of a subpopulation of T cells occurs in
some children with autism, as opposed to healthy children or children with
mental retardation (non-Down's syndrome).
"Deficiency of Suppressor-inducer (CD4+CD45RA+) T Cells in Autism."
Immunological Investigations, vol. 19, number 3, June 1990, pp. 245-51.
Autistic subjects as compared to a group of 35 healthy age-matched subjects had
a significantly reduced number of lymphocytes, a decreased number of CD2+ T
cells and reduced numbers of CD4+ and CD4+CD45RA+ lymphocytes. Results suggest
that an alteration in the suppressor-inducer T-cell subset is associated with
"CD4+ Helper T Cell Depression in Autism." Immunology Letters,
vol. 25, number 4, September 1990, pp. 341-5. Autistic subjects had a
significantly lower percentage and number of CD4+ cells, a lower number of T
cells (CD2+ cells) and B cells (CD20+ cells), and a lower percentage and number
of total lymphocytes than siblings and normal subjects. The level of blood
values for female subjects appeared lower than those for males as compared to
normal subjects of the same sex. Results suggest that a decrease in CD4+ cells
is associated with autism.
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