Re: ARICEPT

[Guest guest]

Hi le,

My youngest son was on aricept for two years. We have since weaned off of it

with no ill effects.

In my opinion It did amazing things for him, kind of picked up where

antivirals and SSRI's left off. It truly did " lift the fog " for him.

For my other son, it did little, but that's how it always is with those two

LOL.

Dr. Chez in Chicago (I think) is probably the most visible

neurologist using aricept with autism. Someone is doing a clinical trial, but

darned if

I can remember who. Maybe Mt. Sinai? I'd think the results should be

forthcoming in the near future.

[Guest guest]

THANKS FOR THE INFORMATION. I QUESS EVERYTHING IS TRAIL AND ERROR .

DANIELLE

[Guest guest]

Aricept is a drug used mostly to address the cognitive deficits of people

with alzheimers disease. A phase one clinical trial for the use of Aricept in

children with autism is currently being done at the University of Pittsburgh

School of Medicine. Information is availalbe at clinicaltrials.gov

Here is the link:

Clinical Trial: Drug Treatment for Autism

Hope this helps!

[Guest guest]

I have heard good things. You're right, it is an Alzheimer's drug.

Haven't tried it.

Jane

On Oct 22, 2004, at 12:14 AM, & Becky wrote:

>

>

>

> Anyone heard of/known of anyone using this drug for ASD

> purposes? A mom on another list I'm on reports semi-miraculous

> speech/language gains after being on it (her son, that is) for just a

> few weeks. It's an Alzheimers drug, I believe.

>

> Just curious,

>

> Becky

>

>

>

[Guest guest]

----Original Message Follows----

From: " & Becky " <beckeric@...>

>Anyone heard of/known of anyone using this drug for ASD purposes? A mom on

>another list I'm on reports semi-miraculous speech/language gains after

>being on it (her son, that is) for just a few >weeks. It's an Alzheimers

>drug, I believe.

>Just curious,

>Becky

I don't know of anyone using Aricept aka Donepezil, but based on various

research I personally wouldn't be comfortable using these type of drugs in a

developing brain without knowing what the long term results could be. We're

only beginning to learn what cholinesterase inhibiting pesticides can

do to the developing brain.

Cheryl

Exp Neurol. 2004 Aug;188(2):461-70.

Cholinesterase inhibitors modify the activity of intrinsic cardiac neurons.

Darvesh S, Arora RC, E, Magee D, Hopkins DA, Armour JA.

Department of Medicine (Neurology), Dalhousie University, Halifax, Nova

Scotia, Canada. sultan.darvesh@...

Cholinesterase inhibitors used to treat the symptoms of Alzheimer's disease

(AD) inhibit both acetylcholinesterase (AChE) and butyrylcholinesterase

(BuChE), albeit to different degrees. Because central and peripheral

neurons, including intrinsic cardiac neurons located on the surface of the

mammalian heart, express both BuChE and AChE, we studied spontaneously

active intrinsic cardiac neurons in the pig as a model to assess the effects

of inhibition of AChE compared to BuChE. Neuroanatomical experiments showed

that some porcine intrinsic cardiac neurons expressed AChE and/or BuChE.

Enzyme kinetic experiments with cholinesterase inhibitors, namely,

donepezil, galantamine, (+/-) huperzine A, metrifonate, rivastigmine, and

tetrahydroaminoacridine, demonstrated that these compounds differentially

inhibited porcine AChE and BuChE. Donepezil and (+/-) huperzine A were

better reversible inhibitors of AChE, and galantamine equally inhibited both

the enzymes. Tetrahydroaminoacridine was a better reversible inhibitor of

BuChE. Rivastigmine caused more rapid inactivation of BuChE as compared to

AChE. Neurophysiological studies showed that acetylcholine and

butyrylcholine increase or decrease the spontaneous activity of the

intrinsic cardiac neurons.

Donepezil, galantamine, (+/-) huperzine A, and tetrahydroaminoacridine

changed spontaneous neuronal activity by about 30-35 impulses per minute,

while rivastigmine changed it by approximately 100 impulses per minute. It

is concluded that (i) inhibition of AChE and BuChE directly affects the

porcine intrinsic cardiac nervous system, (ii) the intrinsic cardiac nervous

system represents a suitable model for examining the effects of

cholinesterase inhibitors on mammalian neurons in vivo, and (iii) the

activity of intrinsic cardiac neurons may be affected by pharmacological

agents that inhibit cholinesterases.

PMID: 15246845 [PubMed - indexed for MEDLINE]

Hum Mutat. 2004 Nov;24(5):408-16.

A paradigm for single nucleotide polymorphism analysis: The case of the

acetylcholinesterase gene.

Hasin Y, Avidan N, Bercovich D, Korczyn A, Silman I, Beckmann JS, Sussman

JL.

Department of Molecular Genetics, Weizmann Institute of Science, Rehovot,

Israel.

Acetylcholinesterase (AChE) plays a crucial physiological role in

termination of impulse transmission at cholinergic synapses through rapid

hydrolysis of acetylcholine. It is a highly conserved molecule, and only a

few naturally occurring genetic polymorphisms have been reported in the

human gene. The goal of the present study was to make a systematic effort to

identify natural single nucleotide polymorphisms (SNPs) in the human ACHE

gene. To this end, the genomic coding sequences for acetylcholinesterase of

96 unrelated control individuals from three distinct ethnic groups were

analyzed. A total of 13 ACHE SNPs were identified, 10 of which are newly

described, and five that should produce amino acid substitutions [c.101G>A

(p.Arg34Gln), c.169G>A (p.Gly57Arg), c.1031A>G (p.Glu344Gly), c.1057C>A

(p.His353Asn), and c.1775C>G (p.Pro592Arg)]. Population frequencies of 11 of

the 13 SNPs were established in four different populations: African

Americans, Ashkenazi Jews, Sephardic Jews, and Israeli Arabs; 15 haplotypes

and five ethnospecific alleles were identified. The low number of SNPs

identified until now in the ACHE gene is ascribed to technical hurdles

arising from the high GC content and the presence of numerous repeat

sequences, and does not reflect its intrinsic heterozygosity. Among the SNPs

resulting in an amino acid substitution, three are within the mature

protein, mapping on its external surface: they are thus unlikely to affect

its catalytic properties, yet could have antigenic consequences or affect

putative protein-protein interactions.

Furthermore, the newly identified SNPs open the door to a study of the

possible association of AChE with deleterious phenotypes-such as adverse

drug responses to AChE inhibitors employed in treatment of Alzheimer

patients and hypersensitivity to pesticides. Hum Mutat 24:408-416, 2004. ©

2004 Wiley-Liss, Inc.

PMID: 15459952 [PubMed - in process]

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