Hard to read, sorry for some reason when I post on my laptop it goes LOOONNGG!!!
Added links to each of the documents to read easier!
This is choppy to get through as it cuts in and out and is kinda long but very interesting on Mycoplasmas, Chronic Infections, etc, talks about Lyme too and is categorized as Biowarfare agent!
-------------------- Seeking renewed health & vitality. --------------------------------- Do not take anything I say as medical advice - I am NOT a dr! Posts: 830 | From TN | Registered: Aug 2007
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bettyg
Unregistered
posted
cj,
how long is this?
do you have dialup or SUPER FAST? ********************************
thanks! for 7 minutes of footage, it takes my dialup 90 minutes to load!
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posted
It is about an hour long, would be torture on dial up I would say!!!!
It is very, very interesting and explains clearly why our situation is so difficult. It goes into mycoplasms, vaccines, gulf war illness, etc, it includes some interesting facts on Lyme as well stating that 26% of ALS is actually linked to Lyme Disease and that up to 90% of ALS is actually linked to mycoplasm.
On Lyme specific states that Lyme patients have high incidence of mycoplasma as well, cannot recall exact %. Also comment that Lyme patients typically have up to 11 infections, that is what it said 11!!!!!!
It is a presentation from the the Institue of Molecular Medicine at the Lay Institute. The Institue of Molecular Medicine has reports on their site that are included in the presentation, maybe that would be a better avenue for you.
-------------------- Seeking renewed health & vitality. --------------------------------- Do not take anything I say as medical advice - I am NOT a dr! Posts: 830 | From TN | Registered: Aug 2007
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Neurodegenerative diseases are chronic degenerative diseases of the Central Nervous System that often cause dementia. Although for the most part the causes and mechanisms of this
collection of brain diseases are not well known, they are increasing in incidence in the developed as well as the underdeveloped world and are often found in the aging population.
These diseases are characterized by molecular changes in nerve cells that result in nerve cell degeneration and ultimately nerve dysfunction and cell death, resulting in neurological signs
and symptoms and in extreme cases dementia. There appears to be a genetic link to neurodegenerative diseases, but the genetic changes that occur and the changes in gene expression that are found in these diseases are
complex. One of the types of change found in essentially all neurological degenerative diseases is the over-expression of oxidative free radical compounds (oxidative stress) that
cause lipid, protein and genetic structural changes. In addition to genetics and changes in gene expression, it is thought that nutritional deficiencies, head trauma, environmental toxins, chronic bacterial and viral infections,
autoimmune immunological responses, vascular diseases, accumulation of fluid in the brain, changes in neurotransmitter concentrations and other causes are involved in various neurodegenerative diseases.
Amyothrophic Lateral Sclerosis (ALS)
ALS, also known as Lou Gehrig's Disease, in a progressive neurodegenerative disease of the upper and lower motor neurons located in the mid-brain, brainstem and spinal cord. In ALS the motor neurons in these areas become
dysfunctional and slowly die, and when this occurs the muscles can no longer receive nerve impulses from the brain. The muscles then weaken and atrophy, resulting eventually in muscle paralysis. ALS patients progress rather
quickly, and only 5% of ALS patients survive beyond 5 years after their diagnosis. The diagnosis of ALS is performed by neurologists and generally follows a set of signs and
symptoms, but there are atypical ALS cases that do not follow the usual clinical course and do not show all of the typical signs and symptoms of classical ALS.
The cause(s) of ALS remain unknown, but there are several new avenues of research that could be important in the development of new treatments for ALS. One theory of ALS is that
an important neurotransmitter, glutamate, is over-expressed resulting in damage to motor neurons and eventually death. There are drugs that can reduce the damage caused by excess glutamate, but these usually only result in a 2-
3 month increase in life span. Newer drugs are being investigated that could slow the effects of glutamate on motor neurons.
Chronic bacterial and viral infections that invade the brain have been found at high incidence in ALS patients, and these may play an important role in nerve cell death. For
example, investigations at the Institute for Molecular Medicine have found that 85% of ALS patients (and 100% of Gulf War veterans with ALS) have bacterial infections caused by
Mycoplasma species (see the publications below). In addition, other bacteria, such as the Lyme Disease Borrelia burgdorfii may also be involved in some patients. These small intracellular bacteria may cause nerve cell
death by increasing the cellular concentration of Reactive Oxygen Species (ROS), free radicals that can damage nerve membrane lipids and proteins and DNA, resulting in apoptosis or programmed cell death. Studies on ALS have
shown that a major defect in ALS is the reduction or change in an enzyme called superoxide dysmutase (SOD) that is involved in reducing the concentration of ROS. In addition,
other studies have shown the reduction over time of of the body's antioxidant defense system in ALS patients. Methods are being developed to treat these infections and also reduce the
generation of ROS by administration of antioxidants and replacing damaged membrane lipids (Lipid Replacement Theray). In addition, neurotrophic viruses such as the Echo-7
enteroviruses are found in most ALS patients, and these viruses could cause cell death to infected cells.
In addition to neurotransmitters and infections, chemical toxins and heavy metals, such as lead, mercury and aluminum may damage nerves and contribute to neurodegeneration. Although ALS is not generally thought to be an
autoimmune disease, several studies have found antibodies to motor neuron membrane components in ALS patients. These autoantibodies may damage nerve cells similar to MS.
Alzheimer's Disease (AD) Alzheimer's Disease (AD), the most common cause of dementia, is a collection of brain disorders, usually in older people, characterized by slow
progressive loss of brain function, especially notable by lapses in memory, disorientation, confusion, mood swings, changes in personality, language problems, such as difficulty in finding
the right words for everyday objects, loss of behavioral inhibitions, loss of motivation, and paranoia. The prognosis and course of AD varies widely, and the duration of illness can be a few
years up to over 20 years in duration. During this time parts of the brain that control memory and thinking are first affected, followed by other brain changes that ultimately result in brain cell death.
AD is characterized by distinct neuropathological changes in the brain. Among the most notable are the appearance of plaques and tangles of neurofibrils within brain nerves
that affect nerve synapses and nerve-nerve cell communication. Both of these structures involve the deposition of altered amyloid proteins, called Ab proteins, and scientists in the Department of Immunology at the Institute for Molecular Medicine are developing new
immunological methods to prevent the deposition of Ab proteins and increase their removal from nerve cells so that the nerve damaging structures are reduced or prevented from forming.
Although the cause of AD is not known to any certainty, formation of the amyloid plaques and neurofiber tangles may be due to genetics and changes in the structure of Ab proteins, neurotoxicity caused by chemicals or other toxic
events, imflammatory responses, oxidative stress and increases in ROS, loss of nerve trophic factors that are important in nerve physiology and loss of nerve cell transmission. Treatments
for AD are generally only palliative and only slow progression of the disease. As mentioned above, newer approaches at the Institute for Molecular Medicine's Department of Immunology have focused on preventing the formation of
amyloid plaques and neurofibril tangles using unique molecular vaccines primed to specific segments on the Ab proteins. These vaccines are currently being studied in animal models of AD,
and clinical trials are being planned to test their effectiveness in patients with AD.
Multiple Sclerosis (MS)
Multiple Sclerosis is a disease of the nerves of the central nervous system, and it can occur in young as well as older people. The nerves in
various parts of the brain are covered by a protective insulation made up of the protein myelin and other proteins imbedded in a lipid sheath so that the electrical impulses that
cause nerve conduction are protected. In MS, inflammation and the presence of autoimmune antibodies against myelin and other antigens causes the protective sheath to break down and
lose their protective capacity (demyelination), resulting in decrease or loss of electrical impulses along the nerve. In progressive MS the nerve cells are damaged by demyelination and
deposition of plaques on the nerve cells to the point where nerve cell death occurs.
The signs and symptoms of MS include visual disturbances, muscle weakness, fatigue, numbness, difficulty in coordinating movement
and balance, tremors, dizziness, loss of hearing, memory loss, impairment in judgment, behavioral changes and pain. The symptoms may cycle or relapse-remit initially and later on
become progressive and degeneration occurs in a steady decline. MS may affect virtually any myelinated nerve, sensory or motorneuron, and it can cause widespread signs and symptoms.
Since MS is a genetic and an autoimmune disease; however, most treatments are specifically directed at symptom relief and some have focused on suppressing the immune response
to nerve cell proteins such as myelin basic protein. Corticosteroids, such as prednisone, are often used, but their non-specific nature can cause side effects related to loss of immune
function. Other approaches have utilized interferons, such as interferon-b1, protein messengers that immune and other cells use to communicate with each other, in an effort to
regulate the immune system and prevent attacks on nerve cell proteins like myelin.
Recent research at the Institute for Molecular Medicine and elsewhere has shown that some of the autoimmune response to nerve cell proteins may be caused by intracellular infections. As
many as 50% of MS patients may be infected with intracellular bacterial infections caused by Mycoplasma species. Other bacterial infections, such as Borrelia burgdorfii (Lyme Disease),
Chlamydia pneumoniae and other intracellular bacterial infections may also be involved in some MS cases. Viruses may also be involved in MS, because certain viruses have been found at
high incidence in MS patients. Infections can stimulate immunological responses, and the presence, in particular, of intracellular bacterial infections in nerve cells can
stimulate autoimmune responses when these intracellular bacteria are released from nerve cells carrying nerve cell antigens.
Autistic Spectrum Disorders (ASD)
Autism patients are young children to teens who generally suffer from an inability to properly communicate, form relationships with others and
respond appropriately to their environments. Autism patients often display repetitive actions and develop troublesome fixations with specific objects, and they are often sensitive to certain
sounds, tastes and smells. Autism patients do not all share the same signs and symptoms but tend to share certain social, communication, motor and sensory problems that affect their
behavior in predictable ways. Autism and related disorders have been recently placed into a multi-disorder category called Autistic Spectrum Disorders (ASD), which includes autism,
Attention Deficit Disorder (ADD) Attention Deficit Hyperactivity Disorder (ADHD), Asperger Syndrome and other disorders.
ASD patients, in general terms, share the presence of a triad of impairments in social interaction, communication and imagination, which are thought to be due to abnormalities in
brain function or structure and are thought to have a genetic basis. The incidence of ASD is currently estimated at 1 in 1,000 children, and in genetically predisposed families the disorder
is ~100-times higher in incidence than in the general population. In some patients there are also a number of other less specific chronic signs and symptoms. Among these are fatigue, headaches, gastrointestinal and vision problems and occasional intermittent low-grade fevers and
other signs and symptoms that are generally excluded in the diagnosis of ASD. These suggest that a subset of ASD patients may suffer from bacterial and/or viral infections. There are
several reasons for this, including the nonrandom or clustered appearance of ASD, sometimes in immediate family members or particular regions, the presence of certain
signs and symptoms associated with infection, the cyclic course of the illness and in some cases its response to anti-microbial therapies.
At the Institute for Molecular Medicine we have identified systemic infections, such as those produced by Mycoplasma species, Chlamydia
pneumoniae and Human Herpes Virus-6 (HHV-6), in a high percentage of ASD patients, and these infections are likely to be important in determining the treatment strategies for many
ASD patients. These infections can penetrate the CNS and are associated with other neurological diseases. In addition, heavy metal contamination, chemical and environmental
exposures also appear to be important in ASD. Since these infections can cause neurological signs and symptoms, they may be important in ASD. Previously we found that children of Mycoplasma-positive Gulf War veterans were over 18-times more likely to come down with Mycoplasma fermentans than the general population and high rates of ASD diagnoses were found in their children. In addition, examination of a group of autism patients from civilian families revealed that there was a high incidence of mycoplasmal infections, including
M. fermentans, M. pneumoniae and M. hominis as well as co-infections with C. pneumoniae or HHV-6, suggesting that chronic infections are common in ASD patients and should be effectively treated.
Systemic intracellular bacterial infections (Mycoplasma, Chlamydia, Borrelia species) in neurodegenerative (MS, ALS) and behavioral disorders (ASD), by Prof. Garth Nicolson, Infectious Disease Newsletter, 2007 (high res)- pdf doc
Evidence for Mycoplasma, Chlamydia pneunomiae and HHV-6 Co-infections in the blood of patients with Autism Spectrum Disorders, Journal of Neuroscience Research, 2007; 85:in press. pdf doc
Ab-immunotherapy for Alzheimer's Disease using mannan-amyloid-beta peptide immunoconjugates, by by A. Ghochikyan, I. Petrushina, A. Lees, V. Vasilevko, N. Movsesyan, et al., DNA and Cell Biology 2006; 25: 571-580. pdf doc
Inflammatory changes parallel the early stages of Alzheimer disease, by A. Parachikova, M.G. Agadjanyan, D.H. Cribbs, M. Blurton-Jones, et al., Neurobiology of Aging 2006; pdf doc
Prototype Alzheimer's disease epitope vaccine induced storng Thy2-type anti-Ab antibody response with alum to Quil A adjuvant switch - by Ghochikyan et al., Vaccine 2006; 24: 2275-2282.- pdf doc
Prototype Alzheimer's Disease vaccine using the immunodominant B cell epitope from beta-amyloid and promiscuous T cell epitope pan HLA DR-binding peptide - by Agadjanyan et al., Journal of Immunology 2005; 174: 1580-1586. - pdf doc
Chronic Mycoplasmal Infections in Gulf War Veterans' Children and Autism Patients by G.L. Nicolson et al., Medical Veritas 2005; 2:383-387. pdf doc
Importance of IgG2c isotype in the immune response to beta-amyloid in amyloid precursor protein/transgenic mice, by I. Petrushina, M. Tran, N. Sadzikava, A. Ghochikyan et al., Neurosciences Letters 2003; 338: 5-8. pdf doc
Generation and characterization of the humoral immune response to DNA immunization with a chimeric beta-amyloid-interleukin-4 minigene, by A. Ghochikyan, V. Vasilevko, I. Petrushina, N. Movsesyan, et al., European Journal of Immunology 2003; 33: 3232-3241. pdf doc
Chronic Mycoplasmal Infections in Autism Patients - by Nicolson et al., Proc. Intern. Mind of a Child Conference, Sydney, Australia 2002 - rtf doc
High frequency of systemic infections in Gulf War veterans and civilians with Amyotrophic Lateral Sclerosis (ALS), by G.L. Nicolson et al., Journal of Clinical Neurosciences 2002; 9:525-529. pdf doc
-------------------- Seeking renewed health & vitality. --------------------------------- Do not take anything I say as medical advice - I am NOT a dr! Posts: 830 | From TN | Registered: Aug 2007
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posted
Of real interest here, they go into mycoplasma and difficulty in tx Lyme because 60%+ with Lyme also has myco's. They use ILADS guidelines but expand a bit because of myco's. Worth the read time.
-------------------- Seeking renewed health & vitality. --------------------------------- Do not take anything I say as medical advice - I am NOT a dr! Posts: 830 | From TN | Registered: Aug 2007
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just don
Frequent Contributor (1K+ posts)
Member # 1129
posted
I would sure like to read this but scrolling so far back and forth for such a LONG post isnt in the cards for me. Would a tiny url help this??
Maybe its MY puter,who knows but great info,just NOT reaqdable!!
-------------------- just don Posts: 4548 | From Middle of midwest | Registered: May 2001
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-------------------- Seeking renewed health & vitality. --------------------------------- Do not take anything I say as medical advice - I am NOT a dr! Posts: 830 | From TN | Registered: Aug 2007
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sparkle7
Frequent Contributor (5K+ posts)
Member # 10397
posted
This is good info but there are tests available for mycoplasmas. It's best to get tested before thinking you have to treat a mycoplasma infection.
I had 2 tests for mycoplasmas & they were both negative.
It's good that he lists Lyme in regards to being a bioweapon. Not many doctors are willing to take the leap.
I think it's necessary, otherwise, how are we going to find a cure? If people are unwilling to accept that what we are dealing may be a bio-engineered weapon - how can we ever find a way to treat it?
Posts: 7772 | From Northeast, again... | Registered: Oct 2006
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Melanie Reber
Frequent Contributor (5K+ posts)
Member # 3707
posted
Hi CJ,
I think it is the line in your second to last post that is causing the WIDE page format.
Thanks for the information. M
Posts: 7052 | From Colorado | Registered: Mar 2003
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posted
still didnt work....guess just do the links instead
-------------------- Seeking renewed health & vitality. --------------------------------- Do not take anything I say as medical advice - I am NOT a dr! Posts: 830 | From TN | Registered: Aug 2007
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posted
Deleted text on the tx guidelines, so youll have to read through the link but it fixed the screen issues. I really believe this may be an answer we are looking for and potentially an answer for our insurance coverages for treatments.
-------------------- Seeking renewed health & vitality. --------------------------------- Do not take anything I say as medical advice - I am NOT a dr! Posts: 830 | From TN | Registered: Aug 2007
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