Archive for the ‘Alzheimer’s’ Category

Are Infections Seeding Some Cases of Alzheimer’s Disease?

https://www.nature.com/articles/d41586-020-03084-9

Are infections seeding some cases of Alzheimer’s disease?

A fringe theory links microbes in the brain with the onset of dementia. Now, researchers are taking it seriously.

Some scientists think that microbes such as the herpes simplex virus 1 (shown here on an epithelial cell) could trigger some cases of Alzheimer’s disease. Credit: SPL

Two years ago, immunologist and medical-publishing entrepreneur Leslie Norins offered to award US$1 million of his own money to any scientist who could prove that Alzheimer’s disease was caused by a germ.

The theory that an infection might cause this form of dementia has been rumbling for decades on the fringes of neuroscience research. The majority of Alzheimer’s researchers, backed by a huge volume of evidence, think instead that the key culprits are sticky molecules in the brain called amyloids, which clump into plaques and cause inflammation, killing neurons. (See link for article)

_____________________

**Comment**

Important quote:

Several microbes have been proposed as triggers of Alzheimer’s, including three human herpes viruses and three bacteria: Chlamydia pneumoniae, a cause of lung infections; Borrelia burgdorferi, the agent of Lyme disease; and, most recently, Porphyromonas gingivalis, which leads to gum disease. In theory, any infectious agent that can invade the brain could have this trigger role (there’s no good evidence, however, that SARS-CoV-2, the virus behind COVID-19, has this ability).

It’s also sad that Alzheimer’s research has been pigeon-holed for so long:  https://madisonarealymesupportgroup.com/2020/01/05/the-maddening-saga-of-how-an-alzheimers-cabal-thwarted-progress-toward-a-cure-for-decades/,  https://madisonarealymesupportgroup.com/2020/01/14/what-causes-alzheimers-not-toxic-amyloid-new-study-suggests/

This article contains Norrins’ paper in the comment section. The article above states there are 40 studies in the cue vying for the 1 million cash prize in March, when the challenge results will be announced:  https://madisonarealymesupportgroup.com/2019/12/23/a-turning-point-in-alzheimers-disease-microbes-matter/

https://madisonarealymesupportgroup.com/2019/12/23/a-turning-point-in-alzheimers-disease-microbes-matter/

Can Lyme Disease Cause Dementia?

https://danielcameronmd.com/can-lyme-disease-cause-dementia/

CAN LYME DISEASE CAUSE DEMENTIA?

can lyme disease cause dementia

There have been reports of Borrelia burgdorferi (Bb), the bacterial agent of Lyme disease, triggering primary dementia, such as Alzheimer’s disease. Researchers who examined the records of 1,594 patients with dementia found that 1.25% had a positive intrathecal anti-Borrelia antibody index (AI), specific for neuroborreliosis. They concluded,

“Pure Lyme dementia exists and has a good outcome after antibiotics.” 1

In a retrospective study, entitled “Secondary dementia due to Lyme neuroborreliosis,” Kristoferitsch and colleagues describe several case reports of patients diagnosed with dementia-like syndromes due to Lyme neuroborreliosis or Lyme disease.2

Rapid improvement with antibiotic treatment

The authors’ case report featuring a 76-year-old woman demonstrates how Lyme disease can cause dementia-like symptoms. The patient developed progressive cognitive decline, loss of weight, nausea, gait disturbance and tremor over a 12-month period. She was referred to a neurology clinic for evaluation.

Three months earlier, the woman had been diagnosed with tension headaches and a depressive disorder. Medications, however, did not improve her symptoms.

Further testing revealed bilateral white matter lesions and an old lacunar lesion located at the left striatum. Extensive neurocognitive testing found “a severe decline of attention, memory and executive functions corresponding to subcortical dementia,” the authors write.

“LNB [Lyme neuroborreliosis] was diagnosed when further CSF [cerebral spinal fluid] examinations disclosed a highly elevated Bb-specific-AI indicating local intrathecal Bb-specific antibody synthesis,” Kristoferitsch writes.

After a 3-week course of treatment with ceftriaxone, the woman “recovered rapidly,” the authors write.

“In a telephone call in February 2018 at the age of 82 years, the patient reported no gait problems or cognitive impairment and had just returned from a trip to Cuba,” the authors write.

Woman admitted to psychiatric ward with severe dementia

A 71-year-old woman with rapidly progressing dementia and short periods of altered consciousness was admitted to a psychiatric hospital. Six months earlier, she was having mild forgetfulness.

MRI results, which indicated slight mesiotemporal atrophy, along with neurocognitive testing supported an initial diagnosis of primary dementia.

“Later, the patient’s daughter reported a tick bite followed by a widespread rash,” the authors write. “Thus, LNB [Lyme neuroborreliosis] was suspected and confirmed by CSF investigations.”

After 2 weeks of antibiotic treatment with ceftriaxone, the woman’s symptoms subsided and her cognition improved.

READ MORE: 80-year-old man with Lyme encephalopathy instead of dementia

At her 5-year follow-up visit, the woman’s “cognition was stable” and memory tests indicated a score above the mean for females her age, “which strongly argued against any dementing process,” the authors write.

In reviewing the literature, Kristoferitsch et al. identified several signs and symptoms that may indicate that Lyme neuroborreliosis (or Lyme disease) is causing dementia in a patient.

Distinguishing features of Lyme-induced dementia

  • Most of the patients or family members did not recall previous tick bites, an EM rash or symptoms of Lyme disease. Therefore, when “EM or other characteristic symptoms of early LB 1–2 years before the onset of dementia may if untreated serve as an indicator for chronic LNB.”
  • Unlike most neurodegenerative dementias, dementia caused by Lyme disease appears to progress rapidly, the authors write.
  • Weight loss is another symptom observed in LNB [Lyme neuroborreliosis],” the authors explain. “It is also compatible with the diagnosis of AD [Alzheimer’s disease] but when it occurs in chronic LNB, it can be more pronounced, reaching up to 20 kg/year.” Weight loss in patients with Alzheimer’s disease is less prominent, the authors explain.
  • Headache, nausea, malaise and vomiting are typically not symptoms of degenerative dementias, the authors explain. But, “might be associated with secondary dementia and thus also with chronic LNB [Lyme neuroborreliosis].”
  • Gait disturbances at the onset or early in the disease which was observed in all cases of this study, makes the diagnosis of a probable AD [Alzheimer’s disease] uncertain or unlikely.”

Additionally, “In most patients, improvement of symptoms was reported already within a few days of antibiotic treatment,” Kristoferitsch writes.

Early recognition and treatment is important

The authors stress the importance of recognizing Lyme-induced dementia-like syndromes.

“It is essential to be aware of this manifestation of Lyme neuroborreliosis, because early antibiotic treatment will prevent permanent sequelae that may occur throughout the further course of the untreated disease,” the authors conclude.

References:
  1. Blanc F, Philippi N, Cretin B, et al. Lyme neuroborreliosis and dementia. J Alzheimers Dis. 2014;41(4):1087-1093. doi:10.3233/JAD-130446
  2. Kristoferitsch W, Aboulenein-Djamshidian F, Jecel J, et al. Secondary dementia due to Lyme neuroborreliosis. Wien Klin Wochenschr. 2018;130(15-16):468-478. doi:10.1007/s00508-018-1361-9

____________________

**Comment**

The proof is in the pudding. These patients were given treatment and they immediately improved. This is noted again and again with chronic Lyme patients – yet according to mainstream medicine led by the CDC and IDSA, this is a figment of our imaginations – otherwise known as PTLDS, an acronym they give complicated cases so they don’t have to deal with persistent infection, and therefore lengthy treatment.

It also allows them to continue to attempt to peddle their lucrative vaccine they continue to pull out of the hat every couple of years.

For more:  https://madisonarealymesupportgroup.com/2020/05/16/lyme-disease-awareness-month-kris-kristofferson-was-misdiagnosed-with-alzheimers-memory-loss-was-due-to-ticks/

For more:  

 

 

Lyme Disease Awareness Month: Kris Kristofferson Was Misdiagnosed With Alzheimer’s, Memory Loss Was Due to Ticks

https://meaww.com/kris-kristofferson-lyme-disease-awareness-misdiagnosed-with-alzheimers-memory-loss-ticks-symptoms

Lyme Disease Awareness Month: Kris Kristofferson was misdiagnosed with Alzheimer’s, memory loss was due to ticks

Kris had been complaining to doctors about memory loss said his wife Lisa Meyers in 2016, ‘That was a big clue to me that maybe it was not really Alzheimer’s’


                            Lyme Disease Awareness Month: Kris Kristofferson was misdiagnosed with Alzheimer's, memory loss was due to ticksKris Kristofferson (Getty Images)

 

The tick-borne illness affects many people but isn’t easily or efficiently diagnosed, with its array of symptoms, it can also be misdiagnosed.

Renowned songwriter and actor and country legend Kris Kristofferson contracted the disease and it went undiagnosed for years. Kristofferson is known for his roles as Rudy Martin in ‘Fast Food Nation’ and songs like ‘Me and Bobby McGee,’ and his suffering shocked many people. (See link for article)

__________________

**Comment**

Kristofferson had a laundry-list of symptoms indicative of tick-borne illness.

What’s truly unfortunate is that there are plenty more out there suffering from the exact same thing to this day who could get better but doctors are woefully ignorant.

For more:  

Reevaluating the Microbial Infection Link to Alzheimer’s Disease

https://www.ncbi.nlm.nih.gov/pubmed/31796672/

2020;73(1):59-62. doi: 10.3233/JAD-190765.

Reevaluating the Microbial Infection Link to Alzheimer’s Disease.

Abstract

 Alzheimer’s disease (AD) is the most common cause of dementia. Despite substantial investment in research, there are no current effective treatments to prevent or delay the onset and development of AD and the exact molecular mechanism of AD pathogenesis is still not fully understood. Researchers have long suspected that microbial infections may play a role in AD; however, this hypothesis has been greatly overlooked for decades, only recently gaining a traction and recognition within the broad scientific community due to new overwhelming evidence on the association of various pathogenic microbes and AD.

Here, we provide our perspective on the significance of these findings, which shed light on the interplay between molecular self-assembly, neurodegeneration, and antimicrobial peptides, as well as propose an amendment to the amyloid cascade hypothesis. It is important to note that this association does not yet prove a causal link, but these reports warrant a thorough investigation into the microbial infection-AD hypothesis which might in turn deliver the elusive therapeutic target the scientific community has been so desperately searching for.

__________________

**Comment**

Perfect example of what happens when the scientific community puts blinders on – they miss things. When science becomes little more than a “good old boy club,” everyone else suffers.  Nowhere is this more evident than in Lyme/MSIDS disease research.

https://madisonarealymesupportgroup.com/2017/01/13/lyme-science-owned-by-good-ol-boys/

https://madisonarealymesupportgroup.com/2019/06/28/who-owns-the-elisa-patents/

https://madisonarealymesupportgroup.com/2019/07/16/another-propaganda-paper-by-auwaerter-more-conflicts-of-interest/ Of note, Auwaerter is on the scientific advisory committee of Diasorin, a company that makes diagnostic tests for Lyme as well as EBV  https://www.diasorin.com/en/node/8937.

This is important as many Lyme/MSIDS patients have both diseases and is a conflict of interest.  https://madisonarealymesupportgroup.com/2017/04/11/diagnosed-with-ebv-had-lyme/

In 1970 DiaSorin began the development of Infectious Disease products designed for use with ELISA technology. Since 2001 it has launched a broad array of new CLIA products, with unique infectious disease assays for use on the LIAISON® systems.

All DiaSorin Infectious Disease products are registered in compliance with the European CE mark rules with commercially available assays in the US having FDA clearance.

Why the Medical Community’s Perspective on Lyme Disease is Different From a Pathologist’s Perspective

Just a year ago I posted a short letter by microbiologist Tom Grier to governors and congressmen in Lyme endemic regions.  You can read it here:  https://madisonarealymesupportgroup.com/2019/08/25/open-letter-to-governors-congressmen-in-lyme-endemic-areas/  Today I post his lengthier letter explaining the state of affairs in simple lay-man’s terms that can be understood by all.  This is a wonderful resource for you to save and refer to when explaining the science behind this horribly mishandled 21st century plague.

LTR to Congress (Letter here)

Executive summary:

  1. Lyme disease is a collection of many species of bacteria, not just borrelia burgdorferi (Bb).
  2. Current testing uses only this one strain (B-31) therefore missing many cases. B-31 is not found in nature and is a created lab strain designed for cost, convenience, & consistency.
  3. Researchers are discovering approximately one new species a year to the existing 17 pathogenic borrelia species.
  4. There are numerous reasons patients are not testing positive on antibody testing such as: low infection load, different borrelia species, immune system ineffectiveness, borrelia quickly moves out of the blood stream and into  human cells.
  5. It can take less than a day for Lyme to get into the brain.
  6. Mouse models show spirochetes entering tissues within minutes.
  7. Some species of Borrelia settle in the brain where it is safe behind the blood brain barrier which prevents drugs from entering.
  8. Borrelia forms protective biofilms also impeding antimicrobials from working.
  9. Brain-autopsies on dementia patients almost always show Borrelia in amyloid plagues.  
  10. Borrelia infections can survive in a dormant state for decades.
  11. Regarding testing, each lab has a different cut off point for dilution.
  12. Independent researchers have found there are more false negatives than false positives.
  13. There are rife conflicts of interests within the CDC regarding Lyme testing as they own the patents.
  14. Borrelia Miyamotoi (Bm) can be transmitted in 20 minutes and autopies show it loves the human brain, and is associated with Alzheimer’s Dementia.
  15. Although Bm is similar to Bb, testing won’t pick it up.
  16. The CDC ignores the shortcomings of testing, the newer species of Borrelia, as well as Lyme-like diseases typically found in the South, and continues to use a one-size-fits-all approach.

I will add to this list the fact that the CDC besides only looking at one strain of borrelia, refuses to acknowledge coinfection involvement of other pathogens which research has shown to complicate cases making them more severe and of longer duration:  https://madisonarealymesupportgroup.com/2019/09/05/babesia-subverts-adaptive-immunity-and-enhances-lyme-disease-severity/

Nearly every patient I work with is coinfected with numerous pathogens yet the CDC/NIH/IDSA refuse to acknowledge this.  Researchers also are finding that ticks are also coinfected:  https://madisonarealymesupportgroup.com/2017/05/18/powassan-and-bb-infection-in-wisconsin-and-u-s-tick-populations/

https://madisonarealymesupportgroup.com/2019/07/28/coinfection-of-many-types-of-borrelia-rickettsia-babesia-bartonella-anaplasma-in-french-castor-bean-ticks/

https://madisonarealymesupportgroup.com/2019/04/26/three-strains-of-borrelia-other-pathogens-found-in-salivary-glands-of-ixodes-ticks-suggesting-quicker-transmission-time/ Another false notion is that ticks have a “grace period” in which they don’t seemingly transmit infections to humans.  This is asinine.  Ticks often feed partially and then drop off.  The pathogens are right in the salivary glands ready to be transmitted to the next unlucky host.

We’ve been sold a bill of lies and the mythology continues unabated.