The Fathers Too, Were Much Older Than Average --A study of classical autism in 1980

1: J Autism Dev Disord. 1980 Sep;10(3):293-7. Links
Maternal age and infantile autism.Gillberg C.
In a total population survey of childhood psychosis in the region of Goteborg, 20 children (2 in every 10,000) fulfilled the diagnostic criteria for infantile autism formulated by Rutter. There was a male preponderance with 15 boys and 5 girls. Eighty-five percent of the mothers were older than average. Mean maternal age in the autistic sample was 30.7 years, compared with 26.0 years in the general population. The difference is statistically significant at the .1% level. There was a strong tendency toward increasing risk of autism in the child with increasing maternal age. The fathers too were much older than average.PMID: 6927656 [PubMed - indexed for MEDLINE]

Newborns At Risk for Special Ed-Fathers 40 or More at birth

1: Eur J Paediatr Neurol. 2007 Mar 6; [Epub ahead of print] Links
Newborns at risk for special education placement: A population-based study.Mannerkoski MK, Aberg LE, Autti TH, Hoikkala M, Sarna S, Heiskala HJ.
Department of Child Neurology, Hospital for Children and Adolescents, Helsinki University Central Hospital, Helsinki, Finland.

OBJECTIVES: To establish the contributions of birth weight (BW), gender, socioeconomic status (SES), and parental age on risks for special education (SE) placements in school-age children. METHODS: A population-based sample of 900 school-age children attending the following full-time SE groups: at level 1, children had isolated neurodevelopmental, physical, or other impairments; at level 2, borderline to mild intellectual disability (ID); and at level 3, moderate to severe ID. Three hundred and one children enrolled in mainstream education formed the control group (level 0). For all children with siblings, we defined familiar forms of learning disorders as having a sibling in one of the SE groupings. We performed our analysis for the entire cohort as well as comparing risk factors within the familial and non-familial types of SE groupings. RESULTS: In multinomial logistic regression analysis, age of father 40 years, low BW (<2500g or <-2 SD), male sex, and parent's lower SES, all increased the probability of SE placement. In the familial forms of levels 2 and 3, the parental SES was lower and, in addition, in the level 2, the family size was bigger. Furthermore, in the non-familial form of level 2, both the low and the high (4000g) BW were more common. CONCLUSIONS: Among the known risk factors for learning disabilities (LD), our study highlighted the importance of a higher paternal age and a lower SES especially in the familial forms of LD.

PMID: 17346999 [PubMed - as supplied by publisher]

FATHER'S AGE AND DEVASTATING DISORDERS

"Until recently, health care professionals have focused almost exclusively on the mother's age as a risk factor for health problems in the child. But we now know that the father's age also adds to the risk of potentially devastating diseases. And there is no practical way to detect these illnesses during pregnancy. For those weighing the risks, the decision can be wrenching. Adoption and in some instances a sperm donation may be acceptable alternatives to older fathers wanting to build a healthy family."

Michael Craig Miller, M.D. is Editor in Chief of the Harvard Mental Health Letter. He is also associate physician at Beth Israel Deaconess Medical Center and assistant professor at Harvard Medical School. He has been practicing psychiatry for more than 25 years and teaches in the Harvard Longwood Psychiatry Residency Program.

Later Paternal Age Can Influence Neural Functioning

Finally, we examined if paternal age was related to the risk for autism in our cohort. We found very strong effects of advancing paternal age on the risk for autism and related pervasive developmental disorders (Reichenberg et al., in press). Compared to the offspring of fathers aged 30 years or younger, the risk was tripled for offspring of fathers in their forties and was increased fivefold when paternal age was >50 years. Together, these studies provide strong and convergent support for the hypothesis that later paternal age can influence neural functioning. The translational animal model offers the opportunity to identify candidate genes and epigenetic mechanisms that may explain the association of cognitive functioning with advancing paternal age.

One Problem--YOU CAN'T CURE AUTISM

CSHL is pursuing a $200 million capital campaign to fund such ventures as the construction of new research facilities dedicated to the study of autism.



The Simons Foundation is a private family foundation based in New York City. The primary mission is to fund advanced research in science and mathematics. A secondary mission is to help children with learning differences. Bridging these two areas, the Simons Foundation has recently undertaken a major initiative supporting research into autism and its treatment. The Foundation aims to spend $100 million long-term to find a cure for the developmental disorder.

Gerald D. Fischbach, M.D., Scientific Director of the Simons Foundation

Gerald D. Fischbach

Gerald D. Fischbach, M.D., is Executive Vice President for Health and Biomedical Sciences; Dean of the Faculties of Health Sciences and Dean of the Faculty of Medicine at the College of Physicians and Surgeons of Columbia University. Dr. Fischbach received his M.D. degree in 1965 from Cornell University Medical School and interned at the University of Washington Hospital. He began his research career at the National Institutes of Health, serving from 1966-1973. He subsequently served on the faculty of Harvard Medical School, first as Associate Professor of Pharmacology from 1973-1978 and then as Professor until 1981. From 1981-1990, Dr. Fischbach was the Edison Professor of Neurobiology and Head of the Department of Anatomy and Neurobiology at Washington University School of Medicine. In 1990, he returned to Harvard Medical School where he was the Nathan Marsh Pusey Professor of Neurobiology and Chairman of the Neurobiology Departments of Harvard Medical School and Massachusetts General Hospital until 1998. He served as Director of the National Institute of Neurological Disorders and Stroke, National Institutes of Health from 1998-2001.





NIH's Gerald D. Fischbach,Named Columbia's Vice President for Health and Biomedical Sciences






Gerald D. Fischbach

Gerald D. Fischbach, M.D., Director of the National Institute of Neurological Disorders and Stroke at the National Institutes of Health (NIH), has been named Columbia University's Vice President for Health and Biomedical Sciences, Dean of the Faculty of Health Sciences and Dean of the Faculty of Medicine, Columbia President George Rupp announced Tues., Dec. 5. Fischbach will also be the Harold and Margaret Hatch Professor of the University in the Faculties of Health Sciences and of Medicine.

A pioneering researcher Fischbach was the Nathan Marsh Pusey Professor of Neurobiology and Chairman of the Neurobiology Departments at both the Harvard Medical School and Massachusetts General Hospital before assuming his current position at NIH in 1998.

At Columbia he will head a division that includes four health science professional schools with 27 academic departments, 3,000 students and 2,300 full-time faculty; a biotechnology park; some 40 biomedical research and treatment centers; and physician practice affiliations with two dozen hospitals. The Health Sciences Division has an annual operating budget of $815 million and has $230 million in sponsored research grants.

Fischbach replaces Herbert Pardes, M.D., who left Columbia in December 1999

THE CREATION OF A DNA DATABANK WILL ONLY BENEFIT THE POCKETS OF THE INVESTORS AND SCIENTISTS AND COMPANIES INVOLVED AND DO NOTHING FOR AUTISTICS

Grant to Yale from Simons Foundation to explore genetic causes of autism
Researchers at the Yale School of Medicine Child Study Center and 10 other institutions will share a $10 million gift from James and Marilyn Simons of The Simons Foundation to create a databank of DNA samples from autism patients around the country.

The goal is to collect a total of 3,000 samples from autism patients around the country to help identify different variants of autism and develop treatments. The principal investigators at Yale, Ami Klin and Matthew State, M.D., have received $1.2 million for three years to collect DNA samples from patients completing clinical evaluations or research protocols at the Autism Program at the Yale Child Study Center.

Autism is a complex brain disorder that inhibits a person’s ability to communicate and develop social relationships, and it is often accompanied by extreme behavioral challenges. Autism Spectrum Disorders are diagnosed in one in 150 children in the United States and affects four times as many boys as girls. Researchers do not know how many subtypes of autism exist. Klin, the Harris Associate Professor of Child Psychology and Psychiatry at Yale, said the gene data might help identify meaningful subtypes of autism, thus advancing knowledge that is critical for behavioral and brain studies, and promoting treatments that will likely be more specific to an individual’s variant of autism.

Other universities participating in the DNA databank collection include Harvard, Columbia, Emory, McGill, Boston, Washington University, the University of Washington, the University of Illinois-Chicago and the University of California, Los Angeles.

The Simons Consortium represents the most comprehensive and detailed effort to date to relate genotypic and phenotypic data in autism. Subjects completing the protocol will have the most refined genotypic analyses that can then be related to a wealth of data on the affected individuals themselves and on their family members. The Consortium will house the data in a centralized repository that will be accessible to researchers within and outside the institutions involved in this effort.

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The Simons Foundation is a private family foundation based in New York City. The primary mission is to fund advanced research in science and mathematics. A secondary mission is to help children with learning differences. Bridging these two areas, the Simons Foundation has recently undertaken a major initiative supporting research into autism and its treatment. The Foundation aims to spend $100 million long-term to find a cure for the developmental disorder.


James Simons

Complex mathematical theories are reborn as investment strategies at Renaissance Technologies. The hedge fund manager, which has some $12 billion in assets under management, focuses on using computer technical models to predict the movement of markets; many of the firm's analysts hold Ph.Ds in math or science disciplines (including astrophysics). Renaissance Technologies was founded by Jim Simons, a former MIT and Harvard math professor who, despite his relative anonymity, ranks among the world's highest-paid hedge fund managers. (Simons is known in mathematical circles as co-author of the Chern-Simons Invarients, used in theoretical physics.)




James H. Simons

Simons is President and founder of Renaissance Technologies Corp. Prior to his financial career, Dr. Simons served as chairman of the Mathematics Department at S.U.N.Y. Stony Brook, taught mathematics at M.I.T. and Harvard University, and was a cryptanalyst at the Institute of Defense Analyses in Princeton, N.J. Dr. Simons’ scientific work was in the area of geometry and topology, and his most influential work involved the discovery and application of certain measurements, now called the Chern-Simons Invariants, which have had wide use, particularly in theoretical physics. James Simons holds a B.S. from MIT, a Ph.D. from U.C. Berkeley, and won the American Mathematical Society’s Veblen Prize for his work in geometry in 1975. He is a former Chairman of the Stony Brook Foundation, and is currently a trustee of Rockefeller University, MIT, and the Institute for Advanced Study.

HOW AUTISM RESEARCH DOLLARS BENEFIT VENTURE CAPITALISTS AND WILL DO NOTHING TO PREVENT AUTISM OR HELP THOSE ALREADY BORN WITH THE DISORDER

The findings could help to determine the risk of having a second child with autism, and the knowledge of which genes are involved may lead to the development of new therapies. NOT UNLESS THEY USE MICRO ARRAY TECHNOLOGY ON THE DNA OF THE SPERM AND SPERMATAGONIA OF THE FATHERS

"This work received the vast bulk of its funding from the Simons Foundation, which generously supported the research when it was little more than an idea and a technique," Wigler said.

Supporters of the research included the Simons Foundation, the National Institute of Mental Health, Autism Speaks, Cure Autism Now, and the Southwestern Autism Research and Resource Center.

"This discovery sets a new framework for understanding, diagnosing and potentially treating autism," said CSHL President Bruce Stillman.

CSHL is pursuing a $200 million capital campaign to fund such ventures as the construction of new research facilities dedicated to the study of autism.


THIS MONEY WILL ONLY BENEFIT INVESTORS/WHO WILL CREATE MORE MONEY FOR THEMSELVES

SOME SPORADIC AUTISM CAN BE PREVENTED IF MEN FATHER ALL THEIR BABIES BY 30 AND CRYOPRESERVE SEMEN IN CLIENT DEPOSITOR SPERM BANK ACCOUNTS. THIS WILL DO MORE GOOD FOR SPORADIC GENETIC DISORDERS SUCH AS ALZHEIMER'S, AUTISM, SCHIZOPHRENIA, PROSTATE CANCER, DIABETES1, MS, ACUTE LYMPHOBLASTIC LEUKEMIA, DUCHENNES MUSCULAR DYSTROPHY, HEMOPHILIA, PRE-MENOPAUSAL BREAST CANCER, FRAGILE-X, RETINOBLASTOMA, ETC. ETC.

Will Researchers Look For Copy Number Variations in the Sperm Making Cells of Fathers of children with CNVs?

The groundbreaking research finding CNVs in some children with sporadic autism has been published. Will the researchers look at the sperm and spermatagonia of the fathers of these children along with all the other fathers and control group?


67.

Vorstman JAS, Staal WG, van DE, van EH, Hochstenbach PFR,
Franke L: Identification of novel autism candidate regions
through analysis of reported cytogenetic abnormalities
associated with autism. Mol Psychiatry 2006, 11:18-28.
This paper summarized chromosome regions known to be associated
with autism phenotype. 15q11.2, 2qter and 22qter represent the most
frequent loci.
68.

Jacquemont M-L, Sanlaville D, Redon R, Raoul O,
Cormier-Daire V, Lyonnet S, Amiel J, Le MM, Heron D,
De Blois M-C et al.: Array- based comparative genomic
hybridization identifies high frequency of cryptic
chromosomal rearrangements in patients with syndromic
autism spectrum disorders. J Med Genet 2006, 43:843-849.
The authors used 1 Mb array CGH to screen 29 patients with autism
spectrum disorders and identified eight clinically relevant genomic rearrangements.
69.

Sebat J, Lakshmi B, Malhotra D, Troge J, Lese-Martin C, Walsh T,
Yamrom B, Yamron B, Yoon S, Krasnitz A et al.: Strong
association of de novo copy number mutations with autism.
Science 2007, in press.
The application of a genome-wide array CGH with 85 000 oligonucleotide
probes (ROMA) (see [27]) in 165 families with autism showed a statistically
significant association of de novo CNV.