MOTOR NEURON, ALS, ALZHEIMER'S, MEMORY CONSULTATION, LYME DISEASE.
There are some cases of Amyotrophic Lateral sclerosis (ALS)- Motor Neuron Disease, linked to Lyme disease. We need to find out what percentage of ALS is caused by Borrelia Burgdorferi. ALS was also caused by Treponema pallidum.
DNA or RNA-s of various viruses and bacteria can bind DNA of host cell nuclei
and can have various effects on host cell functions. There are many data published, but we need much more data and research with respect Borrelia Burgdorferi DNA.
References with respect to ALS and Borrelia burgdorferi
Lancet. 1987 Aug 8;2
(8554):332-3.
Borrelia burgdorferi antibodies and amyotrophic lateral sclerosis.
Waisbren BA, Cashman N, Schell RF,
Johnson R.
Muscle Nerve. 2009 Oct;40(4):626-8.
Lyme disease serology in amyotrophic lateral sclerosis.
Qureshi M,
Bedlack RS, Cudkowicz ME.
Source
Neurology Clinical Trials Unit, Massachusetts General Hospital, Harvard Medical
School, 13th Street, Building 149, Room 2274, Charlestown, Massachusetts 02129, USA.mqureshi@partners.org
Abstract
Lyme disease is sometimes part of the differential diagnosis for amyotrophic lateral sclerosis (ALS). Herein we report on 414 individuals with ALS at the Massachusetts General Hospital who underwent laboratory testing for Lyme disease.
Twenty-four (5.8%) were seropositive, but only 4 (0.97%) had confirmed past immunoreactive infection. Two of these patients received ceftriaxone for 1 month without clinical improvement. Lyme disease was rare in 414 patients with ALS and is not likely to be causative.
Wien Med Wochenschr. 1995;145(7-8):186-8.
[ALS-like sequelae in chronic
neuroborreliosis].
[Article in German]
Hänsel Y, Ackerl M, Stanek G.
Source
Neurologischen Abteilung des Kaiser-Franz-
Josef-Spitals, Wien.
Abstract
CSF investigation in a 61-year old female patient with clinical picture of motoneuron
disease gave evidence for chronic infection with Borrelia burgdorferi. Improvement of clinical and CSF findings could be observed after antibiotic therapy. The diagnosis of amyotrophic lateral sclerosis which was initially suspected had to be revised and the disorder was interpreted as chronic neuroborreliosis.
Rev Neurol (Paris). 2006 Jun;162 Spec No 2:
4S50-4S56.
[What is the role of other complementary examination in amyotrophic lateral sclerosis?].
[Article in French]
Tranchant C.
Source
Département de Neurologie, Hôpitaux Universitaires, Strasbourg. Christine.Tranchant@chru-strasbourg.
fr
Abstract
Amotrophic lateral sclerosis diagnosis is based on clinical and electrophysiological findings. Transcranial
magnetic stimulation and MRI can show abnormalities which are not specific, but which can confirm upper motor neuron involvement. The other tests are performed to exclude differential diagnosis. Tests which should be performed in every cases are: medullar MRI, blood counts, erythrocyte sedimentation, serum protein electrophoresis, calcium, phosphore,
serological tests for HIV, siphylis, Lyme disease. Other tests are made in some clinical circonstances to exclude genetical disease or metabolic disorders (SMN gene, Kennedy gene, Hexosaminidase A, very long chaine fatty acids), haematological or paraneoplasic disorders (anti-neurons antibodies, PSA, CT of chest and abdomen, mammography, bone
marrow biopsy) or inclusion myositis (muscle biopsy).
Wien Med Wochenschr. 1995;145(7-8):186-8.
[ALS-like sequelae in
chronic neuroborreliosis].
[Article in German]
Hänsel Y, Ackerl M, Stanek G.
Source
Neurologischen Abteilung des Kaiser-
Franz-Josef-Spitals, Wien.
Abstract
CSF investigation in a 61-year old female patient with clinical picture of motoneuron disease gave evidence for chronic infection with Borrelia burgdorferi. Improvement of clinical and CSF findings could be observed after antibiotic therapy. The diagnosis of amyotrophic lateral sclerosis which was initially suspected had to be revised and the disorder was interpreted as chronic neuroborreliosis.
PMID: 7610670 [PubMed -
indexed for MEDLINE]
Arch Neurol. 1990 May;47(5):586-94.
Immunologic reactivity against Borrelia burgdorferi in
patients with motor neuron disease.
Halperin JJ, Kaplan GP, Brazinsky S, Tsai TF, Cheng T, Ironside A, Wu P, Delfiner
J, Golightly M, Brown RH, et al.
Source
Department of Neurology, State University of New York, Stony Brook 11794.
Abstract
Of 19 unselected patients with the diagnosis of amyotrophic lateral sclerosis (ALS) living in Suffolk County, New York (an area of high Lyme disease prevalence), 9 had serologic evidence of exposure to Borrelia burgdorferi; 4 of 38 matched controls were seropositive. Eight of 9 seropositive patients were male (8 of 12 male patients vs 2 of 24 controls). Rates of seropositivity were lower among patients with ALS from nonendemic areas. All patients had typical ALS; none had typical Lyme disease. Cerebrospinal fluid was examined in 24 ALS patients--3 (all with severe bulbar involvement) appeared to have intrathecal synthesis of anti-B burgdorferi antibody. Following therapy with antibiotics, 3 patients with predominantly lower motor neuron abnormalities appeared to improve, 3 with severe bulbar dysfunction deteriorated rapidly, and all others appeared unaffected. There appears to be a statistically significant association between ALS and immunoreactivity to B burgdorferi, at least among men living in hyperendemic areas.
Thanks to Judith Miklossy for the above links
Judith Miklossy website is here
Judith Miklossy is trying to establish an International Research Laboratory in order to continue research in this important field of work.
The President of the foundation, Judith Miklossy, MD, PhD, is one of the pioneers who contributed to this emerging field of research and has more than 30 years of clinical and research experience in Switzerland, in the US and in Canada. details here
'The possibility that microorganisms may play a role in senile plaque formation has been discussed by Fischer, Alzheimer and their colleagues more than a century ago. It has also been known from more than a century that chronic bacterial infection can cause dementia. The spirochete Treponema pallidum in syphilis, can cause slowly progressive dementia, cortical atrophy and amyloid deposition, which revealed to be beta-amyloid. Recently it was shown that other types of spirochetes, including Borrelia burgdorferi, the causative agent of Lyme disease are also able to persist in the brain, and cause dementia, brain atrophy and beta-amyloid deposition. Bacteria, including spirochetes, are powerful stimulators of inflammation and are amyloidogenic and they can initiate and sustain chronic inflammation and amyloid deposition in Alzheimer’s disease. Recent observations also revealed that beta-amyloid, which is the most important biological marker of Alzheimer's disease belongs to the family of antimicrobial peptides (AMP).'
'The goal of the foundation is to support and accelerate this new emerging field of research on Alzheimer's disease and related chronic inflammatory disorders. Some pathogens have been already analyzed and serological and diagnostic tests for their detection are commercially available. Others still need to be characterized in order to detect and eradicate them.
Treatments presently used for Alzheimer's disease and other chronic inflammatory disorders are mostly symptomatic. Antibiotics and antiviral drugs for the treatment of bacterial and viral infections are available, however, to optimize available treatments and develop new therapies is essential.'
Prevention Alzheimer Foundation/Judith Miklossy
1921 Martigny-Croix, CP 16
1921,
Switzerland
Banque Cantonale du Valais
1950 Sion, Switzerland
IBAN: CH71 0076 5001 0105 7880 3
Account number: 101 057
8803 - 634526
BIC ou SWIFT : BCVSCH2L
DNA or RNA-s of various viruses and bacteria can bind DNA of host cell nuclei
and can have various effects on host cell functions. There are many data published, but we need much more data and research with respect Borrelia Burgdorferi DNA.
References with respect to ALS and Borrelia burgdorferi
Lancet. 1987 Aug 8;2
(8554):332-3.
Borrelia burgdorferi antibodies and amyotrophic lateral sclerosis.
Waisbren BA, Cashman N, Schell RF,
Johnson R.
Muscle Nerve. 2009 Oct;40(4):626-8.
Lyme disease serology in amyotrophic lateral sclerosis.
Qureshi M,
Bedlack RS, Cudkowicz ME.
Source
Neurology Clinical Trials Unit, Massachusetts General Hospital, Harvard Medical
School, 13th Street, Building 149, Room 2274, Charlestown, Massachusetts 02129, USA.mqureshi@partners.org
Abstract
Lyme disease is sometimes part of the differential diagnosis for amyotrophic lateral sclerosis (ALS). Herein we report on 414 individuals with ALS at the Massachusetts General Hospital who underwent laboratory testing for Lyme disease.
Twenty-four (5.8%) were seropositive, but only 4 (0.97%) had confirmed past immunoreactive infection. Two of these patients received ceftriaxone for 1 month without clinical improvement. Lyme disease was rare in 414 patients with ALS and is not likely to be causative.
Wien Med Wochenschr. 1995;145(7-8):186-8.
[ALS-like sequelae in chronic
neuroborreliosis].
[Article in German]
Hänsel Y, Ackerl M, Stanek G.
Source
Neurologischen Abteilung des Kaiser-Franz-
Josef-Spitals, Wien.
Abstract
CSF investigation in a 61-year old female patient with clinical picture of motoneuron
disease gave evidence for chronic infection with Borrelia burgdorferi. Improvement of clinical and CSF findings could be observed after antibiotic therapy. The diagnosis of amyotrophic lateral sclerosis which was initially suspected had to be revised and the disorder was interpreted as chronic neuroborreliosis.
Rev Neurol (Paris). 2006 Jun;162 Spec No 2:
4S50-4S56.
[What is the role of other complementary examination in amyotrophic lateral sclerosis?].
[Article in French]
Tranchant C.
Source
Département de Neurologie, Hôpitaux Universitaires, Strasbourg. Christine.Tranchant@chru-strasbourg.
fr
Abstract
Amotrophic lateral sclerosis diagnosis is based on clinical and electrophysiological findings. Transcranial
magnetic stimulation and MRI can show abnormalities which are not specific, but which can confirm upper motor neuron involvement. The other tests are performed to exclude differential diagnosis. Tests which should be performed in every cases are: medullar MRI, blood counts, erythrocyte sedimentation, serum protein electrophoresis, calcium, phosphore,
serological tests for HIV, siphylis, Lyme disease. Other tests are made in some clinical circonstances to exclude genetical disease or metabolic disorders (SMN gene, Kennedy gene, Hexosaminidase A, very long chaine fatty acids), haematological or paraneoplasic disorders (anti-neurons antibodies, PSA, CT of chest and abdomen, mammography, bone
marrow biopsy) or inclusion myositis (muscle biopsy).
Wien Med Wochenschr. 1995;145(7-8):186-8.
[ALS-like sequelae in
chronic neuroborreliosis].
[Article in German]
Hänsel Y, Ackerl M, Stanek G.
Source
Neurologischen Abteilung des Kaiser-
Franz-Josef-Spitals, Wien.
Abstract
CSF investigation in a 61-year old female patient with clinical picture of motoneuron disease gave evidence for chronic infection with Borrelia burgdorferi. Improvement of clinical and CSF findings could be observed after antibiotic therapy. The diagnosis of amyotrophic lateral sclerosis which was initially suspected had to be revised and the disorder was interpreted as chronic neuroborreliosis.
PMID: 7610670 [PubMed -
indexed for MEDLINE]
Arch Neurol. 1990 May;47(5):586-94.
Immunologic reactivity against Borrelia burgdorferi in
patients with motor neuron disease.
Halperin JJ, Kaplan GP, Brazinsky S, Tsai TF, Cheng T, Ironside A, Wu P, Delfiner
J, Golightly M, Brown RH, et al.
Source
Department of Neurology, State University of New York, Stony Brook 11794.
Abstract
Of 19 unselected patients with the diagnosis of amyotrophic lateral sclerosis (ALS) living in Suffolk County, New York (an area of high Lyme disease prevalence), 9 had serologic evidence of exposure to Borrelia burgdorferi; 4 of 38 matched controls were seropositive. Eight of 9 seropositive patients were male (8 of 12 male patients vs 2 of 24 controls). Rates of seropositivity were lower among patients with ALS from nonendemic areas. All patients had typical ALS; none had typical Lyme disease. Cerebrospinal fluid was examined in 24 ALS patients--3 (all with severe bulbar involvement) appeared to have intrathecal synthesis of anti-B burgdorferi antibody. Following therapy with antibiotics, 3 patients with predominantly lower motor neuron abnormalities appeared to improve, 3 with severe bulbar dysfunction deteriorated rapidly, and all others appeared unaffected. There appears to be a statistically significant association between ALS and immunoreactivity to B burgdorferi, at least among men living in hyperendemic areas.
Thanks to Judith Miklossy for the above links
Judith Miklossy website is here
Judith Miklossy is trying to establish an International Research Laboratory in order to continue research in this important field of work.
Prevention Alzheimer's - International Foundation
The President of the foundation, Judith Miklossy, MD, PhD, is one of the pioneers who contributed to this emerging field of research and has more than 30 years of clinical and research experience in Switzerland, in the US and in Canada. details here'The possibility that microorganisms may play a role in senile plaque formation has been discussed by Fischer, Alzheimer and their colleagues more than a century ago. It has also been known from more than a century that chronic bacterial infection can cause dementia. The spirochete Treponema pallidum in syphilis, can cause slowly progressive dementia, cortical atrophy and amyloid deposition, which revealed to be beta-amyloid. Recently it was shown that other types of spirochetes, including Borrelia burgdorferi, the causative agent of Lyme disease are also able to persist in the brain, and cause dementia, brain atrophy and beta-amyloid deposition. Bacteria, including spirochetes, are powerful stimulators of inflammation and are amyloidogenic and they can initiate and sustain chronic inflammation and amyloid deposition in Alzheimer’s disease. Recent observations also revealed that beta-amyloid, which is the most important biological marker of Alzheimer's disease belongs to the family of antimicrobial peptides (AMP).'
'The goal of the foundation is to support and accelerate this new emerging field of research on Alzheimer's disease and related chronic inflammatory disorders. Some pathogens have been already analyzed and serological and diagnostic tests for their detection are commercially available. Others still need to be characterized in order to detect and eradicate them.
Treatments presently used for Alzheimer's disease and other chronic inflammatory disorders are mostly symptomatic. Antibiotics and antiviral drugs for the treatment of bacterial and viral infections are available, however, to optimize available treatments and develop new therapies is essential.'
Donations to this important field of research are needed - everybody can deduct donations from tax as it is an International Charitable Foundation. If the donation link on the website doesn't work the bank details are also on the website or -
Prevention Alzheimer Foundation/Judith Miklossy
1921 Martigny-Croix, CP 16
1921,
Switzerland
Banque Cantonale du Valais
1950 Sion, Switzerland
IBAN: CH71 0076 5001 0105 7880 3
Account number: 101 057
8803 - 634526
BIC ou SWIFT : BCVSCH2L
