Vaccine Against Alzheimer's Called 'Promising'/ 7 New Abstracts

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July 24, 2001 Search www.feat.org/search/news.asp

SCIENCE

Also These Abstracts:

* Rett Syndrome Gene OK with 59 With Autism

* Famotidine Treatment of Autistic Children

* Genomeceuticals and the Molecular And Immunological

Aspects Of Autism

* Fluoxetine And Autism

* Regional Magnetic Resonance Spectroscopy Of The Brain In

Autistic Individuals

* Borna Disease Virus (BDV) Infection of the Brain

* Neonatal Borna Disease Virus Infection (BDV)

* Borna Disease Virus Infection Of Adult And Neonatal Rats

* Reader’s Posts

Vaccine Against Alzheimer's Called 'Promising'

Researchers working on a vaccine for Alzheimer's disease are optimistic.

[Written by CBC News Online.]

http://cbc.ca/cgi-bin/templates/view.cgi?/news/2001/07/23/alzh_vacc010723

Initial trials on 100 Alzheimer's patients from the United States and

the United Kingdom showed people tolerated the vaccine well.

In trials on mice, the vaccine was able to protect against the disease

if the injection were given at an early age.

In other mice that already had Alzheimer's, the disease was halted or

even reversed.

The research team, from Elan Pharmaceuticals, now plans to test the

vaccine on 375 Alzheimer's patients from across the U.S. and Europe this

year. This is expected to take two years to complete.

This second stage of research will show if the vaccine, called

AN-1792, will help patients with mild to moderate Alzheimer's.

Brain plaques

The researchers say the trials have helped them understand how the vaccine

works to clear amyloid plaques from the brains of patients, and to prevent

additional plaques from forming.

Amyloid plaques are protein deposits which impede and kill nerves in

the brain. They are a common characteristic of Alzheimer's disease but

researchers aren't sure if they're a cause or a result of the illness.

The vaccine is a synthetic form of naturally occurring beta amyloid

protein, the main component of the plaques.

When injected into mice, the compound prompted an immune response that

increased the clearance of amyloid plaques.

Alzheimer's is a degenerative disease of the brain that attacks nerve

cells, causing mental impairment and loss of memory. Worldwide, 22 million

people are expected to develop the condition by the year 2025.

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Rett Syndrome Gene OK with 59 With Autism

No mutations in the coding region of the Rett syndrome gene MECP2 in 59

autistic patients.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_ui

ds=11464249 & dopt=Abstract

1: Eur J Hum Genet 2001 Jul;9(7):556-8

Vourc'h P, Bienvenu T, Beldjord C, Chelly J, Barthelemy C, Muh JP, Andres C.

Laboratoire de Biochimie et Biologie Moleculaire, INSERM U 316, 2 bis Bd

Tonnelle, 37032 Tours Cedex, France.

Autistic disorder is a pervasive developmental disorder considered to

have a multigenic origin. Mental retardation is present in 75% of autistic

patients. Autistic features are found in Rett syndrome, a neurological

disorder affecting girls and associated with severe mental retardation.

Recently, the gene responsible for the Rett syndrome, methyl CpG-binding

protein (MECP2) gene, was identified on the X chromosome by a candidate gene

strategy.

Mutations in this gene were also observed in some mentally retarded

males. In this study we tested MECP2 as a candidate gene in autistic

disorder by a DGGE analysis of its coding region and intron-exon boundaries.

Among 59 autistic patients, 42 males and 17 females, mentally retarded or

not, no mutations or polymorphisms were present in the MECP2 gene.

Taking into account the size of our sample, we conclude that MECP2

coding sequence mutations are not an important factor (less than 5% of

cases) in the aetiology of autistic disorder. PMID: 11464249 [PubMed - in

process]

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Famotidine Treatment of Autistic Children

Famotidine treatment of children with autistic spectrum disorders: pilot

research using single subject research design.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_ui

ds=11459079 & dopt=Abstract

1: J Neural Transm 2001;108(5):593-611

y LA, Tsiouris JA, Cohen IL, Shindledecker R, DeCresce R.

Department of Pediatrics, St. Luke's-Roosevelt Hospital Center, New York,

NY, USA. lal14@...

Using single subject research design, we performed pilot research to

evaluate the safety and efficacy of famotidine for the treatment of children

with autistic spectrum disorders. We studied 9 Caucasian boys, 3.8-8.1 years

old, with a DSM-IV diagnosis of a pervasive developmental disorder, living

with their families, receiving no chronic medications, and without

significant gastrointestinal symptoms.

The dose of oral famotidine was 2 mg/kg/day (given in two divided

doses); the maximum total daily dose was 100 mg. Using single-subject

research analysis and medication given in a randomized, double-blind,

placebo-controlled, cross-over design, 4 of 9 children randomized (44%) had

evidence of behavioral improvement.

Primary efficacy was based on data kept by primary caregivers,

including a daily diary; daily visual analogue scales of affection,

reciting, or aspects of social interaction; Aberrant Behavior Checklists

(ABC, Aman); and Clinical Global Improvement scales. Children with marked

stereotypy (meaningless, repetitive behaviors) did not respond.

Our subjects did not have prominent gastrointestinal symptoms and

endoscopy was not part of our protocol; thus, we cannot exclude the

possibility that our subjects improved due to the effective treatment of

asymptomatic esophagitis. The use of famotidine for the treatment of

children with autistic spectrum disorders warrants further investigation.

PMID: 11459079 [PubMed - in process]

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Genomeceuticals and the Molecular And Immunological Aspects Of Autism.

Application of genomeceuticals to the molecular and immunological aspects of

autism.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_ui

ds=11461171 & dopt=Abstract

1: Med Hypotheses 2001 Jul;57(2):186-91

Brudnak MA. MAK Wood Inc., Thiensville, Wisconsin, USA

Autism is a developmental disease affecting as many as 1 in 300

children and is often characterized as a mental disorder originating in

infancy that is associated with self-absorption, inability to interact

socially, behavior, and language dysfunction (e.g. echolalia). Current

theories indicate an important role of diet in the development of disease.

It is thought that, as a result of maldigestion of casein and gluten,

opioid-type peptides, or exorphins, are produced.

Additionally, because of the time-frame of development of the disease,

there has been an association with childhood vaccination. Consequently,

prevailing therapies attempt to address these causes in one, or a

combination, of three ways: diet restriction (removing casein and gluten);

supplementation with exogenous enzymes; and probiotic bacteria. Until

recently, none of the therapies addressed the molecular mechanisms that may

be at work in the development and progression of autism.

This paper presents potential molecular and cellular mechanism r

elated to autism as well as discusses their application to the treatment of

the disease through the application of genomeceuticals.

Additionally, a link between developmentally associated aberrant

immune and inflammatory responses, and autism is suggested and explored.

Copyright 2001 Harcourt Publishers Ltd.

PMID: 11461171 [PubMed - in process]

* * *

Fluoxetine And Autism

Effect of fluoxetine on regional cerebral metabolism in autistic spectrum

disorders: a pilot study.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_ui

ds=11466160 & dopt=Abstract

1: Int J Neuropsychopharmacol 2001 Jun;4(2):119-25

Buchsbaum MS, Hollander E, Mehmet Haznedar M, Tang C, Spiegel-Cohen J, Wei

TC, Solimando A, Buchsbaum BR, Robins D, Bienstock C, Cartwright C, Mosovich

S.

The regional metabolic effects of fluoxetine were examined in patients

with autism spectrum disorders. Six adult patients with DSM-IV and Autism

Diagnostic Interview (ADI) diagnoses of autism (n = 5) and Asperger's

syndrome (n = 1), entered a 16-wk placebo-controlled cross-over trial of

fluoxetine.

The patients received 18F-deoxyglucose positron emission tomography

with co-registered magnetic resonance imaging at baseline and at the end of

the period of fluoxetine administration. After treatment, the patients

showed significant improvement on the scores of the Yale-Brown

Obsessive-Compulsive Scale - Obsessions subscale and the Hamilton Anxiety

Scale; Clinical Global Impressions - Autism scores showed 3 of the patients

much improved and 3 unchanged. Relative metabolic rates were significantly

higher in the right frontal lobe following fluoxetine, especially in the

anterior cingulate gyrus and the orbitofrontal cortex.

Patients with higher metabolic rates in the medial frontal region and

anterior cingulate when unmedicated were more likely to respond favourably

to fluoxetine. These results are consistent with those in depression

indicating that higher cingulate gyrus metabolic rates at baseline predict

SRI response.

PMID: 11466160 [PubMed - in process]

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* * *

Regional Magnetic Resonance Spectroscopy Of The Brain In Autistic

Individuals.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_ui

ds=11465765 & dopt=Abstract

1: Neuroradiology 2001 Jun;43(6):496-8

Hisaoka S, Harada M, Nishitani H, Mori K.

Department of Radiology, School of Medicine, University of Tokushima, Japan.

We studied the variations in the concentration of metabolites with

brain region and age in autistic individuals and normal controls using

multiple analysis of covariance. We examined 55 autistic individuals (2-21

years old, 47 male and eight female) and 51 normal children (3 months-15

years old, 26 boys and 25 girls). Single volumes of interest were placed in

the frontal, parietal and temporal region on both sides, the brain stem and

cingulate gyrus.

The concentration of each metabolite was quantified by the water

reference method. The concentration of N-acetylaspartate in the temporal

regions (Brodmann's areas 41 and 42) in the autistic individuals were

significantly lower than those in the controls (P < 0.05), but

concentrations in other regions were not significantly different between the

autistic individuals and controls.

This suggests low density or dysfunction of neurones in Brodmann's

areas 41 and 42 in autistic individual, which might be related to the

disturbances of the sensory speech centre (Wernicke's area) in autism.

PMID: 11465765 [PubMed - in process]

* * *

Borna Disease Virus (BDV) Infection of the Brain

Effects of neonatal rat Borna disease virus (BDV) infection on the postnatal

development of the brain monoaminergic systems.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_ui

ds=10675767 & dopt=Abstract

1: Brain Res Dev Brain Res 2000 Feb 7;119(2):179-85

Pletnikov MV, Rubin SA, Schwartz GJ, Carbone KM, Moran TH.

Department of Psychiatry and Behavioral Sciences, The s Hopkins

University School of Medicine, Ross 618, 720 Rutland Avenue, Baltimore, MD

21205, USA. pletnikov@...

Effects of neonatal Borna disease virus infection (BDV) on the

postnatal development of brain monoaminergic systems in rats were studied.

Tissue content of norepinephrine (NE), dopamine (DA) and its metabolite,

3,4-dihydroxyphenol acetic acid (DOPAC), and serotonin (5-HT) and its

metabolite, 5-hydroxyindole-3-acetic acid (5-HIAA) were assayed by means of

HPLC-EC in frontal cortex, cerebellum, hippocampus, hypothalamus and

striatum of neonatally BDV-infected and sham-inoculated male rats of

8, 14, 21, 60 and 90 days of age.

Both NE and 5-HT concentrations were significantly affected by

neonatal BDV infection. The cortical and cerebellar levels of NE and 5-HT

were significantly greater in BDV-infected rats than control animals at

postnatal days (PND) 60 and 90. Tissue content of NE in hippocampus was

unaffected. In hippocampus, neonatally BDV-infected rats had lower 5-HT

levels at PND 8 and significantly elevated levels at PND 21 and onwards.

Neither striatal levels of 5-HT nor hypothalamic levels of 5-HT and

NE were affected by neonatal BDV infection, suggesting that the monoamine

systems in the prenatally maturing brain regions are less sensitive to

effects of neonatal viral infection. 5-HIAA/5-HT ratio was not altered in

BDV-infected rats indicating no changes in the 5-HT turnover in the brain

regions damaged by the virus.

Neither DA nor DOPAC/DA ratio was affected by neonatal BDV infection

in any of the brain regions examined. The present data demonstrate

significant and specific alterations in monoaminergic systems in neonatally

BDV-infected rats. This pattern of changes is consistent with the previously

reported behavioral abnormalities resulting from neonatal BDV infection.

PMID: 10675767 [PubMed - indexed for MEDLINE]

* * *

Neonatal Borna Disease Virus Infection (BDV)

Neonatal Borna disease virus infection (BDV)-induced damage to the

cerebellum is associated with sensorimotor deficits in developing

rats.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_ui

ds=11172881 & dopt=Abstract

1: Brain Res Dev Brain Res 2001 Jan 31;126(1):1-12

Pletnikov MV, Rubin SA, Carbone KM, Moran TH, Schwartz GJ.

Department of Psychiatry and Behavioral Sciences, The s Hopkins

University School of Medicine, Ross 618, 720 Rutland Avenue, Baltimore, MD

21205, USA. mpletnik@... Neonatal

Borna disease virus (BDV) infection of the brain produces

developmental damage to the cerebellum in rats, with minimal classical

inflammatory responses. In the present study, we assessed the consequences

of this damage by measuring motor coordination and postural skills in

developing (postnatal days 4 to 30) rats that were neonatally infected

with BDV.

Neonatal BDV infection-induced motor impairments were selective and

correlated with the time course of BDV damage to cerebellar development.

BDV-induced motor deficits were not seen until the end of postnatal week 2.

By postnatal week 3, BDV-infected rats had deficits in negative geotropism,

fore- and hind limb placing and grasping. BDV-infected rats also exhibited

deficits in the ability to hold on to a bar and to cross a suspended bar.

Neonatal BDV infection induced impairments in the acoustic startle

response. Compared to controls, neonatally BDV-infected rats exhibited

attenuated habituation of the acoustic startle at postnatal day (PND ) 23

and decreased startle responsiveness at PND 30.

Prepulse inhibition of the acoustic startle remained unaltered in

BDV-infected rats. The data demonstrate that neonatal BDV brain infection of

rats can be a valuable animal model system for studying the relationship

between abnormal brain development and resultant behavioral deficits.

Further studies of this model may elucidate specific pathogenic

mechanisms that that may have implications in the study of

neurodevelopmental human disorders.

PMID: 11172881 [PubMed - indexed for MEDLINE]

* * *

Borna Disease Virus Infection Of Adult And Neonatal Rats

Borna disease virus infection of adult and neonatal rats: models for

neuropsychiatric disease.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_ui

ds=11417134 & dopt=Abstract

1: Curr Top Microbiol Immunol 2001;253:157-77

Hornig M, Solbrig M, Horscroft N, Weissenbock H, Lipkin WI.

Laboratory for the Study of Emerging Diseases, 3101 Gillespie Neuroscience

Research Facility, University of California, Irvine, CA 92697-4292, USA.

Animal models provide unique opportunities to explore interactions

between host and environment. Two models have been established based on

Borna disease virus infection that provide new insights into mechanisms by

which neurotropic agents and/or immune factors may impact developing or

mature CNS circuitry to effect complex disturbances in movement and

behavior.

Note in press: Since this chapter was submitted, several manuscripts

have been published that extend findings reported here and support the

relevance of BDV infections of neonatal rats as models for

investigating mechanisms of neurodevelopmental damage in autism. Behavioral

abnormalities, including disturbed play behavior and chronic emotional

overactivity, have been described by Pletnikov et al. (1999);

inhibition of responses to novel stimuli were described by Hornig et

al. (1999);

loss of Purkinje cells following neonatal BDV infection has been

demonstrated by Eisenman et al. (1999), Hornig et al. (1999), and

Weissenbock et al. (2000);

and alterations in cytokine gene expression have been reported by

Hornig et al. (1999), Plata-Salaman et al. (1999) and Sauder et al. (1999).

PMID: 11417134 [PubMed - indexed for MEDLINE]

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Reader’s Posts:

We are the parents of two autistic sons ages 3 and 1. We are interested in

hearing from any parents or doctors on the safety of the Mercury

Detoxification using DMSA. We live in Saginaw, Michigan and would like to

know if there are any doctors in our area who are familiar with this

process.

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Hi, I am interested in the Method in Boston. Has anyone done the Sign

and Spoken language program? Or Symbolic Playthings? How about Overview

with Dr ? Anyone been to the LCDC in Boston? Thanks for the input.

JRae32566@...

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Has anyone had any experience with the Transdermal Secretin? I would like

to know your experiences...Jen JRae32566@...

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