posted
Not a fun read, but consistent with the sense that Chronic Lyme "brainfog" is a very serious symptom, and seriously underexamined by medical researchers.
Judith Miklossy, Kamel Khalili, Lise Gern, Rebecca L. Ericson, Pushpa Darekar, Lorie Bolle, Jean Hurlimann, Bruce J. Paster
Borrelia burgdorferi persists in the brain in chronic Lyme neuroborreliosis and may be associated with Alzheimer's disease
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.
IP: Logged |
bettyg
Unregistered
posted
cod, may I suggest you edit and break up the body text of all the informative info? we neuro lymies can't comprehend that long solid block of text. thank you.
since my sister-in-law died at age 40 of early-onset AD; i have a special interest in this post.
IP: Logged |
CaliforniaLyme
Frequent Contributor (5K+ posts)
Member # 7136
posted
Shirley Forsman Shirley Forsman February 6, 1930 - November 9, 1999
Shirley Forsman was mis-diagnosed with Alzheimer's disease for 9 years before she died of Lyme disease in Pine County, Minnesota.
Many thanks to Lyme Alliance for allowing this excerpt-written by Tom Grier, from their newsletter:
"Shirley Forsman, RN, had a history of Lyme disease at age 59 and was treated with two weeks of Doxycycline. It was about two years later that Shirley was diagnosed with early progressive Alzheimer's disorder and her health steadily and quite rapidly declined. Within a few short years, Shirley needed complete around the clock care that was provided by her daughter, Katie Harp. Shirley was no longer able to walk, talk or perform daily functions such as dressing, having conversations or controlling her bodily functions.
"Always suspecting that her mother's mutli-system problems were caused by unresolved Lyme disease, Katie fought for years to have her tested and treated. Her requests were always met with resistance until she found a young Bemidji internist who was willing to do a trial of IV Rocephin just to see if the patient responded. Amazingly, the patient responded favorably and almost immediately.
After having been nearly completely non-responsive to any outside stimuli for over two years, Shirley was now beginning to recognize family members. She could form sentences that were a few words long and was now standing and walking short distances. In fact, the physician was now recommending physical therapy and a walker.
The most dramatic change was perhaps the change in the frequency and severity of Shirley's seizures. Grand mal seizures could be expected almost every week and they were often violent enough to throw her out of bed. The nightly thrashing and lashing about in her bed came to an abrupt stop shortly after antibiotics were introduced. In the end, Shirley was going as long as two months without any major seizures or bed thrashing. Her muscle twitches in her face were completely gone.
Upon seeing this change in Shirley's health, the attending doctor changed the diagnosis from Alzheimer's to neurological Lyme disease. However, shortly after switching Shirley from her IV Rocephin to a combination of orals, her health began to decline. After a series of seizures, Shirley died at age 69."
Her death certificate lists Cause of Death as: seizure disorder as a complication of Lyme disease.
-------------------- There is no wealth but life. -John Ruskin
All truth goes through 3 stages: first it is ridiculed: then it is violently opposed: finally it is accepted as self evident. - Schopenhauer Posts: 5639 | From Aptos CA USA | Registered: Apr 2005
| IP: Logged |
CaliforniaLyme
Frequent Contributor (5K+ posts)
Member # 7136
posted
June Atkins June Atkins, 77
JUNE L. ATKINS��A memorial service will be held at a later date for June L. Anderson Atkins, 77, Oley, who died July 19, 2000 at the Berkshire Center, 5501 Perkiomen Ave., Exeter Township, where she had been a patient.
She was born in Reiffton and was the wife of George T. Atkins for 45 years. ��Atkins was a graduate of the Reading Hospital School of Nursing and worked at several hospitals before joining the U.S. Navy as an RN. She served at various Naval Hospitals both in the U.S. and overseas and is a Korean War Veteran. She resigned from the Navy as a Lieutenant USN (RN) to become a homemaker.
She was vice president and board member of the Reading Box Co. Inc. ��A member of St. Gabriel's Episcopal Church, Douglassville, she was a Sunday school teacher for many years. ��She belonged to many organizations including the American Legion, Oley Post 878, Historical Society of Berks County, serving for several years as a Docent. She was also vice president of Youth Education Valley Forge Chapter of Freedoms Foundation, for many years. In addition to her husband, she is survived by three children, Lance Atkins, Sinking Springs, Jennifer L. (Atkins) Lehr, Sinking Springs and Brent Atkins, Exeter Township, eight grandchildren and four sisters.
Atkins body is being donated to medical research for study of Vascular Dementia and Lyme Disease from which she died.
In lieu of flowers, donations may be made to the Historical Society of Berks County, 940 Center Ave., Reading, PA 19601
-------------------- There is no wealth but life. -John Ruskin
All truth goes through 3 stages: first it is ridiculed: then it is violently opposed: finally it is accepted as self evident. - Schopenhauer Posts: 5639 | From Aptos CA USA | Registered: Apr 2005
| IP: Logged |
CaliforniaLyme
Frequent Contributor (5K+ posts)
Member # 7136
posted
**************************************
1: Neurobiol Aging. 2006 Feb;27(2):228-36.
Beta-amyloid deposition and Alzheimer's type changes induced by Borrelia spirochetes.
Miklossy J, Kis A, Radenovic A, Miller L, Forro L, Martins R, Reiss K, Darbinian N, Darekar P, Mihaly L, Khalili K. Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3. [email protected]
The pathological hallmarks of Alzheimer's disease (AD) consist of beta-amyloid plaques and neurofibrillary tangles in affected brain areas.
The processes, which drive this host reaction are unknown. To determine whether an analogous host reaction to that occurring in AD could be induced by infectious agents, we exposed mammalian glial and neuronal cells in vitro to Borrelia burgdorferi spirochetes and to the inflammatory bacterial lipopolysaccharide (LPS).
Morphological changes analogous to the amyloid deposits of AD brain were observed following 2-8 weeks of exposure to the spirochetes.
Increased levels of beta-amyloid precursor protein (AbetaPP) and hyperphosphorylated tau were also detected by Western blots of extracts of cultured cells that had been treated with spirochetes or LPS.
These observations indicate that, by exposure to bacteria or to their toxic products, host responses similar in nature to those observed in AD may be induced.
PMID: 15894409 *************************************** Intracranial aneurysms in three patients with disseminated Lyme borreliosis: cause or chance association?
METHODS: Three patients with Borrelia burgdorferi infection and intracranial aneurysms are described.
RESULTS: All three patients had neurological symptoms. Perivascular and vasculitic lymphocytic inflammation were detected in the brain biopsy specimen of one patient. The aneurysm was located in the internal carotid arteries in two patients and in the basilar artery in one patient. The aneurysm ruptured in two patients.
CONCLUSIONS: Cerebral lymphocytic vasculitis and intracranial aneurysms may be associated with B burgdorferi infection. It is suggested that inflammatory changes caused by B burgdorferi in vessel walls may be a pathogenetic mechanism for the formation of aneurysms. *************************************
Vasculitis course of neuroborreliosis with thalamic infarct
Keil R, Baron R, Kaiser R, Deuschl G Nervenarzt 1997 Apr 68:4 339-41
Abstract A-20-year-old man without vascular risk factors presented with paraesthesia of the left side of the body with acute onset. Cerebral magnetic resonance imaging showed an infarction in the right thalamus.
Intra-arterial digital subtraction angiography revealed stenosis of the right thalamic vessels.
Recent infection by Borrelia burgdorferi was demonstrated by typical findings in the cerebrospinal fluid: lymphocytic pleocytosis and intrathecal synthesis of borrelial-specific antibodies. The diagnosis of a borrelial-induced vasculitis with secondary thalamic infarction was made from these findings. After antibiotic treatment with cefrtriaxone, the patient was discharged without residual complaints.
*********************************
Inflammatory brain changes in Lyme borreliosis. A report on three patients and review of literature. Oksi J, Kalimo H, Marttila RJ, Marjam�ki M, Sonninen P, Nikoskelainen J, Viljanen MK Brain 1996 Dec 119 ( Pt 6) 2143-54
Abstract Despite a rapid increase in the number of patients with Lyme neuroborreliosis (LNB), its neuropathological aspects are poorly understood. The objective of this study was evaluation of neuropathological, microbiological, and magnetic resonance imaging (MRI) findings in three patients with the Borrelia burgdorferi infection and neurological disease from whom brain tissue specimens were available. Perivascular or vasculitic lymphocytic inflammation was detected in all specimens. Large areas of demyelination in periventricular white matter were detected histologically and by MRI in one patient.
The disease had a fatal outcome in this patient. Brain MRI suggested malignancies in two patients before histopathological studies were carried out. One of these two patients was a child with sudden hemiparesis. Another was a 40-year-old man presenting with epileptic seizures and MRI-detected multifocal lesions, which disappeared after repeated courses of antibiotics.
We conclude that cerebral lymphocytic vasculitis and multifocal encephalitis may be associated with B. burgdorferi infection. The presence of B. burgdorferi DNA in tissue samples from areas with inflammatory changes indicates that direct invasion of B. burgdorferi may be the pathogenetic mechanism for focal encephalitis in LNB.
************************************************* Retinal vasculitis in Lyme borreliosis. Leys AM, Sch�nherr U, Lang GE, Naumann GO, Goubau P, Honore A, Valvekens F Bull Soc Belge Ophtalmol 1995 259 205-14
Abstract We observed retinal vasculitis in seven patients with clinical and serologic evidence of Borrelia burgdorferi infection.
Three patients presented with abrupt loss of vision due to acute retinal vasculitis.
Funduscopy demonstrated engorged veins, hemorrhages, perivenous infiltrates and retinal white spots. Fluorescein angiography showed leakage from the veins, from the white spots and from the optic disc. Moreover arterial occlusions were observed in two patients. Four patients had signs of chronic uveitis with vitritis, cystoid macular oedema and retinal vasculitis, which was associated with neovascularization and vitreous hemorrhage in one patient, and with optic neuritis in another patient.
Six patients received antibiotic treatment and three patients received systemic corticosteroids.
Marked improvement in the three acute retinal vasculitis cases occurred within several weeks, the fundus changes disappeared in another few months, and no recurrences were observed. The final visual acuity was excellent in these patients, although optic disc pallor and visual field loss persisted in one case. In the four patients with chronic uveitis visual blurring improved following antibiotic treatment and the retinal vasculitis and vitritis slowly regressed. The proliferative retinopathy of one patient required panretinal laser treatment.
-------------------- There is no wealth but life. -John Ruskin
All truth goes through 3 stages: first it is ridiculed: then it is violently opposed: finally it is accepted as self evident. - Schopenhauer Posts: 5639 | From Aptos CA USA | Registered: Apr 2005
| IP: Logged |
posted
Herbs for circulation have helped me (hawthorne, periwinkle, gotu kola), and carnetine and A-L-carnatine.
And killing those darn kootiess!
Susan
Posts: 233 | From United States | Registered: Oct 2006
| IP: Logged |
Greatcod
Unregistered
posted
Lots of good information, thanks. Three things have prompted my deeper interest in Lyme's impact on the brain. One is my own partially improved life..infected for 10 years before diagnosis and treatment, and not likely to ever recover fully. So still Lymebrained is many ways. I know others like me and suspect that there are many many more. Next, the sense that Lyme's cognative effects are vastly under estimated and under studied. I don't think that Klempner's study even attempted to measure the impact of treatment on cognition, and that is the study the "other side" uses as definitive proof that ABX treatment does not work on chronics. Frightening, really. Third is the possibility that Bush is a chronic now, and that, if so, his capacity to make informed decisions is seriously undermined.
IP: Logged |
The Lyme Disease Network is a non-profit organization funded by individual donations. If you would like to support the Network and the LymeNet system of Web services, please send your donations to:
The
Lyme Disease Network of New Jersey 907 Pebble Creek Court,
Pennington,
NJ08534USA http://www.lymenet.org/
UBBFriend: Email this page to someone!
![[Big Grin]](biggrin.gif)
Printer-friendly view of this topic