FEAT DAILY NEWSLETTER
Sacramento, California http://www.feat.org
February 8, 2002
News Morgue Search www.feat.org/search/news.asp
(Abstracts)
·
Secretin Takes Another Research Hit
·
Autistic Traits In Obsessive-Compulsive Disorder.
·
Molecular Genetics And Animal Models In Autistic
Disorder
·
The Amygdala And Related Structures In The Pathophysiology
Of Autism.
·
NIDS National Video Conference February 9th
Saturday
·
Sponsorship Opportunities: Power Of One! I.D.E.A Autism
Awareness Rally
‘A double-blind, placebo-controlled crossover study
investigating the effect of porcine secretin in children with autism.’
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=11824175&dopt=Abstract Corbett B, Khan K, Czapansky-Beilman D, Brady N,
Dropik P, Goldman DZ, Delaney K, Sharp H, Mueller I, Shapiro E, Ziegler R. Department of Pediatrics, Divisions of
Pediatric Neurology, University of Minnesota, Minneapolis, MN, USA.
OBJECTIVES: A recent patient series reported the
incidental findings of improved social and language skills in 3 children with
autistic spectrum disorders after the administration of secretin, a peptide
hormone. However, a subsequent study did not find evidence for a drug effect.
Parents are seeking treatment with secretin despite the absence of empirical investigations
demonstrating amelioration in autism symptomology.
In order to more precisely measure the effects of
secretin, this study investigated the effect of a single intravenous dose of
porcine secretin on 12 autistic children through a randomized, double-blind,
placebo-controlled, crossover study. Children were assessed on objective
language and on social, neuropsychological, and gastrointestinal measures to
evaluate drug effects. The study was
conducted over a 16-week trial.
The results indicated that significant differences were
not observed on the majority of the dependent variables. Statistically significant
differences were observed on measures of positive affect and activity level following
secretin infusion. In general, the autistic children did not demonstrate the
improvements described in the initial retrospective report.
PMID: 11824175 [PubMed - in process]
* * *
Autistic Traits In Obsessive-Compulsive Disorder.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=11827611&dopt=Abstract <- - address ends here. Bejerot S, Nylander L, Lindstrom E.
Department of Neuroscience, Psychiatry, University
Hospital, Uppsala, Sweden.
In contrast to other non-psychotic psychiatric
populations, subjects with obsessive-compulsive disorder (OCD) are more prone
to have personality disorder from cluster A (the odd and eccentric cluster).
The present study aims at further investigating the
relationship between these and other personality traits in OCD subjects and
their relation to high functioning autism (HFA) and Asperger disorder.
Sixty-four subjects with OCD were included. Personality traits were assessed
with the Karolinska Scales of Personality (KSP), and personality disorders with
DSM-adapted questionnaires.
In addition, autistic traits were assessed in 29
videotaped subjects, by 3 independent raters. Twenty percent of the subjects
with OCD were identified as also having autistic traits. These subjects scored
higher on KSP scales measuring muscular tension, psychasthenia, and inhibition
of aggression and lower on socialization as compared with OCD subjects without autistic
traits. Additionally, subjects with autistic traits fulfilled criteria for
anxious personality disorders and paranoid personality disorders significantly
more often than subjects without autistic traits.
We propose that OCD is often related to HFA and
Asperger disorder.
Self-report questionnaires may be useful in establishing
the diagnosis. However, those with the
most obvious autistic features seem to be less able to identify these traits in
themselves.
PMID: 11827611 [PubMed - in process]
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* * *
Molecular Genetics And Animal Models In Autistic Disorder.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=11827743&dopt=Abstract<- - address ends here. Andres C.
INSERM U316, Tours Cedex, France
Autistic disorder is a behavioural syndrome beginning
before the age of 3 years and lasting over the whole lifetime. It is
characterised by impaired communication, impaired social interactions, and
repetitive interests and behaviour. The prevalence is about 7/10,000 taking a restrictive
definition and more than 1/500 with a broader definition, including all the
pervasive developmental disorders.
The importance of genetic factors has been highlighted by epidemiological
studies showing that autistic disorder is one of the most genetic
neuropsychiatric diseases.
The relative risk of first relatives is about 100-fold
higher than the risk in the normal population and the concordance in
monozygotic twin is about 60%. Different strategies have been applied on the
track of susceptibility genes.
The systematic search of linked loci led to contradictory
results, in part due to the heterogeneity of the clinical definitions, to the differences
in the DNA markers, and to the different methods of analysis used. An
oversimplification of the inferred model is probably also cause of our
disappointment.
More work is necessary to give a clearer picture. One
region emerges more frequently: the long arm of chromosome 7. Several candidate
genes have been studied and some gave indications of association: the Reelin
gene and the Wnt2 gene. Cytogenetical abnormalities are frequent at 15q11-13,
the region of the Angelman and Prader-Willi syndrome.
Imprinting plays an important role in this region, no
candidate gene has been identified in autism. Biochemical abnormalities have
been found in the serotonin system. Association and linkage studies gave no
consistent results with some serotonin receptors and in the transporter,
although it seems interesting to go further in the biochemical characterisation
of the serotonin transporter activity, particularly in platelets, easily accessible.
Two monogenic diseases have been associated with
autistic disorder:
tuberous sclerosis and fragile X. A better knowledge of
the pathophysiology of these disorders can help to understand autism. Different
other candidate genes have been tested, positive results await replications in
other samples. Animal models have been developed, generally by knocking out the
different candidate genes. Behaviour studies have mainly focused on anxiety and
learning paradigms. Another group of models results from surgical or toxic
lesions of candidate regions in the brain, in general during development. The
tools to analyse these animals are not yet standardised, and an important
effort needs to be undertaken.
* * *
The Amygdala And Related Structures In The Pathophysiology
Of Autism.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=11830179&dopt=Abstract <- - address ends here. Sweeten TL, Posey DJ, Shekhar A, McDougle
CJ.
Department of Psychiatry, Indiana University School of
Medicine, 541
Clinical Drive, Room 298, 46202-5111, Indianapolis, IN,
USA
Autism is a neurodevelopmental disorder that is defined
behaviorally by severe deficiencies in reciprocal social interaction, verbal
and nonverbal communication, and restricted interests. The amygdala is involved
in the regulation of social behaviors and may be an important site of pathology
for the social dysfunction seen in autism. This review focuses on lesion,
postmortem, and neuroimaging studies that investigate the amygdala and related
structures in this disorder.
Other brain regions potentially involved in the
neuropathology of autism are also briefly discussed. Although supportive
evidence exists for amygdala dysfunction in autism, the currently available
data are inconsistent and additional research is needed.
PMID: 11830179 [PubMed - in process]
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* * *
Autism Spectrum Disorders, PDD-NOS, ADD/ADHD, Chronic
Fatigue Syndrome:
A Medical Epidemic and the Neuro-Immune Connection:
Exciting Update: What Can You DO RIGHT NOW! WHAT DOES THE FUTURE HOLD!
Presentations by members of the NIDS Scientific and
Medical Advisory Board:
Dr. Griffith is a Pediatric Neurologist in practice in
Northern California and affiliated with University of San Francisco. Dr. Griffith
has a patient base comprised mainly of children on the Autism Spectrum. Dr. Griffith’s is an expert is in the area
of neuro-cognitive assessments and therapy
and the understanding of cognitive
evaluation tools to support therapeutic and clinical trials.
Dr. Michael Goldberg, M.D., F.A.A.P., Medical Director,
NIDS Research Institute Scientific & Medical
Advisory Board
Dr. Goldberg received his Medical Degree from UCLA and
trained at
LAC-USC Medical Center. He is the Medical Director of the
NIDS Research Institute Scientific & Medical Advisory Board. He is on the
clinical teaching staff at both UCLA and Cedars-Sinai Hospitals. He has 17
years experience in evaluating and treating children with disorders that fall within
the evolving spectrum of NIDS.
Dr. Jeffery
Galpin M.D.
Dr. Galpin received his Medical Degree from University of
Illinois and trained at Presbyterian St. Luke’s Hospital in Chicago. He also
completed a post-doctoral fellowship at University of California in Infectious
Disease and at the National Institutes of Health. He has received the Young
Research Award for Genetic Engineering and Immunology and is currently an
Associate Professor at the University of Southern California, Chairman of the
Shared Medical Research Foundation, Editor Emeritus of the Infectious Disease
Alert World Newsletter. During his career, his accomplishments include
developing the first gene therapy for AIDS and co-developing Hydroxyurea, a
synergistic drug for AIDS.
Dr. Klimas is currently a Professor of Medicine,
Psychology, Microbiology and Immunology at the University of Miami School of
Medicine and the Miami VA Medical Center. She is also a clinical immunologist
who has worked in the area of neuro-immune connections, in relation to HIV Infections
and Chronic Fatigue Syndrome, for approximately fourteen years. Her work in associating the degree of immune
activation with severity of cognitive dysfunction has led to the study of
potential mechanisms relative to these findings. These laboratory-based
observations are currently being translated into clinical trials that will aid
in finding treatments for symptoms of cognitive dysfunction through
immune-based therapies.
This will be a full day event starting at 8AM/PST (to
accommodate the East Coast till 5PM/PST. We will have presentations followed by
a Round Table Question and Answer period.
The following sites are confirmed:
California University Sites (CSU):
Northridge (Los Angeles)
Bakersfield (Kern County- 100 Miles N of LA)
San Jose State (Just South of San Francisco)
Chico State (If there is interest)
University of California Sites (UC):
UCSF (San Francisco)
UC Irvine (If there is interest)
UC Davis (If there is
interest)
Outside California
University of Arizona, Tucson
Minnesota
Austin, TX (Sponsored by SUN Microsystems)
Washington, DC (The UC Washington Center)
Other Tentative Sites In negotiation are:
University of Washington, Seattle
Saddleback College (Orange County, CA)
University of Texas at San Antonio Medical School
Please send confirmation of attendance with the
specific
location to info@healnids.org
* * *
Sponsorship Opportunities: Power Of One!
I.D.E.A Autism Awareness Rally
[From Unlocking Autism.]
The time for The Power of One! I.D.E.A. Rally is fast
approaching! We have some great things
planned for April 18 - 21, 2002. Check
our website at www.UnlockingAutism.org
on a regular basis for updates on events.
The website will change weekly as we are working diligently on all the
events that will take place for Autism Awareness in Our Nations Capitol.
As many of you know, Unlocking Autism funds most of its
operations on a few small fundraisers hosted by our State Representatives and
through our online sales and
donations. This year, our largest
fundraiser was organized by Geoff Dubrowsky and took place at the Red Mile Run
in Lexington, Kentucky. Through his
tireless dedication and networking with all his friends and colleagues, Geoff
was able to raise an incredible $40,000.
With those funds Unlocking Autism was able to cover all of their expenses
for the event and provide training the
same weekend for 17 Unlocking Autism State Representatives who came from across
the nation. We have also been able to
supply full training packets to the additional 215 Representatives across the
nation and continue developing the many
projects we sponsor.
We have just mailed our initial deposit of $18,000 for the
Rally. An addition $15,000 is due in 15
days. On the day of the Rally we will
have to make a final payment and estimate additional expenses to exceed $15,000.
Because we believe so strongly in the powerful and lasting results these
events will make, we are asking you to join with us by investing in these incredible
event. We are certain that during April
18-21, through the dedication of each of you, much needed National political
changes will happen for each one we love with autism.
Please unite with us by visiting our website to make a
donation or purchase.
We have a limited number of Organizational, Corporate, and
Personal Sponsorships available that are listed below as well. If you, the company you work for, the
organization you belong to or a friend or family member of yours is interested in sponsoring at one of these
levels, please send us an email or call Shelley Reynolds at KEYS2UA@aol.com,
225-769-1532 or Jeana Smith at UnlockAutism@aol.com,
225-791-0231.
Sponsorship Levels For THE POWER OF ONE! I.D.E.A. National Autism
Awareness Rally Washington, DC April 21, 2002
$5,000 For a
sponsorship of $5,000 your company/organization will receive: a) A logo of your
choice on the back of the rally shirt b) A complimentary banner on stage at the
event c) Signage indicating sponsorship at the entrance to the event. d) A
complimentary literature table located on the grounds of the event and a vendor
booth in the vending area. e) Three announcements of recognition during the
event to encourage attendees to visit your booth. f) Sponsorship signage on all
rally flyers distributed prior to April 21 and sponsorship on the home page of
the Unlocking Autism website for the duration of December 31, 2002.
$2500 For a sponsorship of $2,500 your
company/organization will receive: a) Signage indicating sponsorship at the
entrance to the event. b) A complimentary literature table located on the
grounds of the event and a vendor booth in the vending area. c) Two
announcements of recognition during the event to encourage attendees to
visit your booth. d) Sponsorship signage on all rally flyers distributed prior
to April 21 and sponsorship on the home page of the Unlocking Autism website
through April 30, 2002.
$1000 For a sponsorship of $1,000 your
company/organization will receive: a) Signage indicating sponsorship at the
entrance to the event. b) A complimentary literature table located on the
grounds of the event and a vendor booth in the vending area. c) Sponsorship
signage on all rally flyers distributed prior to April 21.
We Sincerely thank you for your support!
Lenny Schafer, Editor@feat.org • CALENDAR EVENTS@feat.org
Michelle Guppy
Catherine Johnson PhD
• Ron Sleith •
Kay Stammers • Edward Decelie
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