posted
I'd be interested in hearing from anyone with first hand experience of Lyme misdiagnosed as Alzheimer's. My main question is in the last sentence. Thank you.
My father was diagnosed with and treated for Lyme disease in 2002 at the age of 76. Around 2004 he began developing memory problems that became obvious around 2006. Today his short term memory is gone. He still recognizes his family but can do nothing for himself.
My sister and I suspected a link to Lyme. Around 2005 his doctors were convinced to do a blood test. It was positive for Lyme antibodies. The reaction was -No reason to treat, the results mean nothing because we know he had Lyme-.
I had Lyme in 1992, all consisting of joint & muscle pain. I also thought that abx treatment was the end of it.
My fathers experience with Lyme involved bad joint & muscle problems no cognitive stuff.
5 years ago when my father was losing his memory I knew nothing of neurological Lyme but now I have been battling it myself for the last 9 months. My experience included short term memory loss and a total out of it foggy disoriented feeling, trouble doing simple tasks, trouble speaking.
My fathers dimentia was not accompanied by The headaches, eye problems, hearing problems that I experienced. These other symptoms were escalating in me so fast at the time I started treatment that they were impossible to ignore.
Does anyone have experience with Lyme that mimics Alzheimer's without the other symptoms?
Posts: 29 | From East Tennessee | Registered: Nov 2010
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posted
There are published reports of a link between cases of Alzheimers and lyme. If you want them, I will try to find a few references.
That does not mean your father's case is caused by lyme, but it would sure be worth checking into. Memory problems are common in lyme. If this were my father I would take him to a lyme doc and see if a trial treatment with antibiotics produced any results. You could try for a PCR or other antigen testing, which looks for the actual germ, not the antibodies (which theoretically could be old, not from current disease.)
And as you may know, there is a lot of variation in lyme symptoms among patients.
Posts: 8430 | From Not available | Registered: Oct 2000
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J Alzheimers Dis. 2008 May;13(4):381-91. Chronic inflammation and amyloidogenesis in Alzheimer's disease -- role of Spirochetes.
Miklossy J.
University of British Columbia, Kinsmen Laboratory of Neurological Research, Vancouver, BC, Canada. Abstract
Alzheimer's disease (AD) is associated with dementia, brain atrophy and the aggregation and accumulation of a cortical amyloid-beta peptide (Abeta). Chronic bacterial infections are frequently associated with amyloid deposition. It had been known from a century that the spirochete Treponema pallidum can cause dementia in the atrophic form of general paresis. It is noteworthy that the pathological hallmarks of this atrophic form are similar to those of AD. Recent observations showed that bacteria, including spirochetes contain amyloidogenic proteins and also that Abeta deposition and tau phosphorylation can be induced in or in vivo following exposure to bacteria or LPS. Bacteria or their poorly degradable debris are powerful inflammatory cytokine inducers, activate complement, affect vascular permeability, generate nitric oxide and free radicals, induce apoptosis and are amyloidogenic. All these processes are involved in the pathogenesis of AD. Old and new observations, reviewed here, indicate that to consider the possibility that bacteria, including several types of spirochetes highly prevalent in the population at large or their persisting debris may initiate cascade of events leading to chronic inflammation and amyloid deposition in AD is important, as appropriate antibacterial and antiinflammatory therapy would be available to prevent dementia.
Med Hypotheses. 2006;67(3):592-600. Epub 2006 May 3. Plaques of Alzheimer's disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete.
MacDonald AB.
St. Catherine of Siena Medical Center, Department of Pathology, 50 Rte 25 A, Smithtown, NY 11787, USA.
Abstract
Here is hypothesized a truly revolutionary notion that rounded cystic forms of Borrelia burgdorferi are the root cause of the rounded structures called plaques in the Alzheimer brain. Rounded "plaques' in high density in brain tissue are emblematic of Alzheimer's disease (AD). Plaques may be conceptualized as rounded "pock mark-like" areas of brain tissue injury. In this century, in brain tissue of AD, plaques are Amyloid Plaques according to the most up to date textbooks. In the last century, however, Dr. Alois Alzheimer did not require amyloid as the pathogenesis for either the disease or for the origin of its plaques. Surely, amyloid is an event in AD, but it may not be the primal cause of AD. Indeed in plaques, amyloid is regularly represented by the "congophilic core" structure which is so named because the waxy amyloid material binds the congo red stain and is congophilic. However an accepted subset of plaques in AD is devoid of a congophilic amyloid core region (these plaques "cotton wool" type plaques, lack a central congophilic core structure). Furthermore, there is "plaque diversity" in Alzheimer's; small, medium and large plaques parallel variable cystic diameters for Borrelia burgdorferi. Perturbations of AD plaque structure (i.e. young plaques devoid of a central core and older plaques with or without a central core structure) offer room for an alternate pathway for explanation of ontogeny of the plaque structures. If amyloid is not required to initiate all of the possible plaques in Alzheimer's, is it possible that amyloid just a by product of a more fundamental primal path to dementia? If a byproduct status is assigned to amyloid in the realm of plaque formation, then is amyloid also an epiphenomenon rather than a primary pathogenesis for Alzheimer's disease. In the "anatomy is destiny" model, cysts of borrelia are always round. Why then not accept roundness as a fundamental "structure determines function" argument for the answer to the mystery of why Alzheimer plaques are always round? Parataxis causality, a concept borrowed from philosophy, is the error that comes from linking two events, which occur contemporaneously or in close proximity to one another with a cause and effect relationship. Parataxis tells us that what appears to be cause and effect in the couplet "amyloid plaque" merely by a proximity relationship may be "spurious causality" which is a cognitive dead end.
PMID: 16675154 [PubMed - indexed for MEDLINE]
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J Alzheimers Dis. 2004 Dec;6(6):639-49; discussion 673-81. Borrelia burgdorferi persists in the brain in chronic lyme neuroborreliosis and may be associated with Alzheimer disease.
University Institute of Pathology, Division of Neuropathology, University Medical School (CHUV), 1011, Lausanne, Switzerland.
Abstract
The cause, or causes, of the vast majority of Alzheimer's disease cases are unknown. A number of contributing factors have been postulated, including infection. It has long been known that the spirochete Treponema pallidum, which is the infective agent for syphilis, can in its late stages cause dementia, chronic inflammation, cortical atrophy and amyloid deposition. Spirochetes of unidentified types and strains have previously been observed in the blood, CSF and brain of 14 AD patients tested and absent in 13 controls. In three of these AD cases spirochetes were grown in a medium selective for Borrelia burgdorferi. In the present study, the phylogenetic analysis of these spirochetes was made. Positive identification of the agent as Borrelia burgdorferi sensu stricto was based on genetic and molecular analyses. Borrelia antigens and genes were co-localized with beta-amyloid deposits in these AD cases. The data indicate that Borrelia burgdorferi may persist in the brain and be associated with amyloid plaques in AD. They suggest that these spirochetes, perhaps in an analogous fashion to Treponema pallidum, may contribute to dementia, cortical atrophy and amyloid deposition. Further in vitro and in vivo studies may bring more insight into the potential role of spirochetes in AD.
sutherngrl
Frequent Contributor (1K+ posts)
Member # 16270
posted
In my state right now there is a doctor doing a study, treating Alzheimer patients with antibiotics. He says it is showing great promise.
I think this says a lot. If not lyme, then some kind of bacterial infection is causing Alzheimers, since it is responding to antibiotics. In your fathers case it sounds like LD.
Posts: 4035 | From Mississippi | Registered: Jul 2008
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posted
Thank you for the replies and for taking the time to look up the detailed information.
Posts: 29 | From East Tennessee | Registered: Nov 2010
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posted
I cannot give you citations but in the documentary Under Our Skin about lyme,
there was a researcher featured who found lyme in around 80% of Alzheimer brain tissue samples.
-------------------- Not everything in life that can be counted counts and not every thing that counts can be counted...Albert Einstein Posts: 208 | From Northeast | Registered: Aug 2010
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t9im
Frequent Contributor (1K+ posts)
Member # 25489
posted
It was Dr. McDonald, a pathologist in NY in under our skin. There is an exerpt on youtube. Sadly he now has Alzheimers.
-------------------- Tim Posts: 1111 | From Glastonbury, CT | Registered: Apr 2010
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