[SarahO]

Hello Peoples*)*!)!!

It won't let me post the ALS Lyme page link so I can't. I will post it in 10 posts*)! Because I am new again here, but I was here for years years ago. There is a IV Rocepihn trial right now where you can get ONE YEAR of IV Rocephin free or placebo unfortunately-

I used to be here years back in the Lyme section- I'm Sarah O aka CaliforniaLyme. I was a neuro mutt, now 100% symptom free, thanks to 9 months of IV Rocepihn. I was, looking back, more Parkie than anything else- I had chorea with athetosis and progressive weakness and choking and bradykinesia and lots of yucky stuff- FMS CFS MCS-

If you are in SANTA CRUZ COUNTY CA that is the #1 place for Lyme disease in CA just fyi-

Take care-
Sarah O

The acamprosate abstract is this-
it could possibly help people with TBE virus induced ALS- or plain ALS
because it is a furin inhibitor!!!!

ANYWAY- it's cheap- it won't hurt- and it COULD HELP!

Consideration of acamprosate for treatment of ALS

1: Med Hypotheses. 2007;69(4):836-7. Epub 2007 Mar 21.

Consideration of acamprosate for treatment of amyotrophic lateral sclerosis.

Kast RE, Altschuler EL. Department of Psychiatry, University of Vermont, College of Medicine, 2 Church Street, Burlington, VT 05401, USA. rekast@email.com


Amyotrophic lateral sclerosis (ALS) is a fatal disease of degeneration of motor neurons. There is no known cure or life extending treatment. Much recent work has suggested that a possible cause of ALS is constitutive opening of the calcium pore in glutamate sensitive AMPA channels secondary to a failure of RNA editing that would change a crucial glutamate in the channel to arginine.


Here, we point out that the small molecule pharmaceutical acamprosate, usually used as a drug to maintain alcohol abstinence, may block this calcium pore--as do the related molecules endogenous polyamines such as putrescine, cadaverine, spermidine and spermine--and thus might have use in ALS.

PMID: 17368956

[SarahO]

because if it's a calcium cascade causing mitochrondrial shutdown it would stop that hypothetically- and in TBE viruses furin also plays a role!!!

what also plays a role in TBE viruses- PH!!!! Alkalinity can potentially inactivate TBE.

I web the ALS/Lyme page and have for years now. We have had 4 ALSers locally come to our group and 3 have lived, although that sounds different than it is. 2 were diagnsoed Lyme THEN ALS, so the TBE variant likelihood was stronger from the get go than for your average ALSer. The third was diagnsoed Lyme & ALS within one day!!! The 4th had been diagnosed ALS for a while and was very late and he died in his second week of IV Rocephin from c difficile.

The 3 that lived- 2 did LEDUM and longterm IV Rocephin and Babesiosis treatment. Why would longterm Babs treatment matter? Babesiosis causes acidosis. TBE viruses are activated by acidity. Therefore it makes sense as to why so many of the Lyme/ALS survivors had longterm Babs treatment.

What is ledum? Ledum is

a. an herb, ledum palustre, used for treating Lyme (yes!)
b. an herb which inactivates TBE viruses (yes!)

why does this matter?

TBE VIRUSES

what do they have to do with ALS???

besides, you may say, we don't HAVE TBE viruses in the USA.

not true. We DO have TBE family viruses in the usa. 2 of them I know of...

a. Powassan
b. "Deer Tick Virus" (sounds like joke but is actual dumb name)

so what the heck is this chick blathering on about TBE & ALS for, you may ask??

This is why-

: Zh Nevropatol Psikhiatr Im S S Korsakova. 1983;83(8):1173-9.
Structure of progressive forms of tick-borne encephalitis

Umanekii KG, Dekonenko EP.

On the basis of long-term follow up (from 2 to 22 years) of 175 patients with various syndromes of progressive forms of tick-borne encephalitis (TBE), evaluation criteria of TBE progression are systematized.

Two basic forms of disease progression are identified: amyotrophic and hyperkinetic, each of them breaking down into a series of leading syndromes. Important for characterizing progressive forms of tick-borne encephalitis (PFTBE) are the time when the disease began to progress and the pattern of progression as well as its stage and severity. PFTBE are correlated with the acute period syndromes.

In long-term follow-up, 68% of patients with PFTBE display transformation of clinical forms of the disease, with

the formation of the lateral amyotrophic sclerosis syndrome

in the overwhelming majority of these patients.


PMID: 6414202

[SarahO]

Reproducing ALS in Lab Animals by Incoulation of Schu Virus Isolated from ALS Patient
Attempts to reproduce amyotrophic lateral sclerosis in laboratory animals by inoculation of Schu virus isolated from a patient with apparent amyotrophic lateral sclerosis
W. K. Müller1, 2 and G. Schaltenbrand1, 2

(1) Laboratorium voor medische Microbiologie der Rijksuniversiteit, Leiden, The Netherlands

(2) Neurologische Universitätsklinik Würzburg, Federal Republic of Germany

(3) Psychiatrisches Landeskrankenhaus, D-6908 Wiesloch, Federal Republic of Germany

Received: 27 January 1978

Summary A virus isolated from the CSF of a patient who had amyotrophic lateral sclerosis for 7 years, and prolonged pleocytosis in the CSF, was adapted to suckling mouse brain by subsequent serial blind passages.

This Schu virus belongs to the tick-borne encephalitis complex of the genus Flavivirus (Togaviridae).

Suckling mouse brain homogenate of the 13th passage was used for transmission experiments in various species of laboratory animals. Golden hamsters infected subcutaneously fell ill after a number of months, lost weight, and had paresis of the legs. Histologically they had petechial hemorrhages in different parts of the CNS and inflammatory changes in the gray substance of the spinal cord.

Pilot studies with repeated inoculations of small doses of different flavivirus strains suggest a course of the disease in experimental animals which resembles slow-virus infections insofar as no encephalitis is produced and degenerative changes of the anterior horn cells prevail over inflammatory signs in the spinal cord.

After intracerebral application of Schu virus, cynomolgus monkeys developed the typical lesions of togavirus panencephalitis with epileptic seizures, ataxia, and paresis. After subcutaneous application, the virus seems to spread along peripheral nerves to anterior spinal roots and spinal cord, where mainly motor neurons of the anterior horn are damaged, and from there to the brain.

The histological findings are such that one may assume the disease of the patient was due to the infection with the virus isolated from his CSF.

Therefore, the hypothesis may be advanced that at least some of the cases diagnosed as amyotrophic lateral sclerosis are due to a togavirus infection.

Key words Amyotrophic lateral sclerosis - Togavirus - Flavivirus - Schu virus - Experimental reproduction of ALS

[SarahO]

70% of ALS in Hamburg, Germany Related to TBE Virus
1: J Neurol 1975 Dec 2;211(1):11-23
An uncommon case of amyotrophic lateral sclerosis with isolation of a virus from the CSF.

Muller WK, Hilgenstock F.

An atypical case of amyotrophic lateral sclerosis (ALS) is described, characterized by early manifestation, a long lasting course with asymmetry of the lesions, absence of bulbar symptoms in the presence of an otherwise very advanced symptomatology, and constant signs of an inflammatory reaction in the CSF which was the reason to initiate extensive virological studies, including procedures for virus isolation.

A virus belonging to the TbE complex of arbovirus group B (tick-borne flavivures), was finally isolated from the CSF.

About 70% of the ALS cases in Hamburg/W. Germany, examined for antibodies, apparently had contact with this virus. The antibody pattern found made it possible to explain this exceptional case.

PMID: 56428