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)
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.
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.
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.
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Lyme disease is a collection of many species of bacteria, not just borrelia burgdorferi (Bb).
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.
Researchers are discovering approximately one new species a year to the existing 17 pathogenic borrelia species.
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.
It can take less than a day for Lyme to get into the brain.
Mouse models show spirochetes entering tissues within minutes.
Some species of Borrelia settle in the brain where it is safe behind the blood brain barrier which prevents drugs from entering.
Borrelia forms protective biofilms also impeding antimicrobials from working.
Brain-autopsies on dementia patients almost always show Borrelia in amyloid plagues.
Borrelia infections can survive in a dormant state for decades.
Regarding testing, each lab has a different cut off point for dilution.
Independent researchers have found there are more false negatives than false positives.
There are rife conflicts of interests within the CDC regarding Lyme testing as they own the patents.
Borrelia Miyamotoi (Bm) can be transmitted in 20 minutes and autopies show it loves the human brain, and is associated with Alzheimer’s Dementia.
Although Bm is similar to Bb, testing won’t pick it up.
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.
Yet, researchers are still at a loss as to why this condition — which is characterized by memory impairment and many other cognitive problems — occurs in the first place. And until they fully understand the cause, investigators will remain unable to devise a cure.
So far, the prevailing hypothesis among experts has been that the excessive accumulation of a potentially toxic protein — beta-amyloid — in the brain causes Alzheimer’s.
Researchers have argued that beta-amyloid plaques disrupt the communication between brain cells, potentially leading to cognitive function problems.
Now, a new study from the University of California San Diego School of Medicine and the Veterans Affairs San Diego Healthcare System suggests that while the buildup of beta-amyloid has associations with Alzheimer’s, it may not actually cause the condition.
In a study paper that appears in the journal Neurology, the researchers explain what led them to reach this conclusion.
“The scientific community has long thought that amyloid drives the neurodegeneration and cognitive impairment associated with Alzheimer’s disease,” says senior author Prof. Mark Bondi.
He notes that “[t]hese findings, in addition to other work in our lab, suggest that this is likely not the case for everyone and that sensitive neuropsychological measurement strategies capture subtle cognitive changes much earlier in the disease process than previously thought possible.”
What comes first?
In their study, the researchers worked with a total of 747 participants with different levels of cognitive health. All of the study participants agreed to undergo neuropsychological assessments, as well as PET and MRI brain scans.
Of the participants, 305 were cognitively healthy, 289 had mild cognitive impairment, and 153 displayed markers of what the investigators call “objectively-defined subtle cognitive difficulties (Obj-SCD).”
Experts define mild cognitive impairment as a state of cognitive impairment that is more severe than what one would normally experience with age, but not yet severe enough for a dementiadiagnosis.
But what are Obj-SCD? In their paper, the investigators define them as “difficulties or inefficiencies on some sensitive cognitive tasks even though the overall neuropsychological profile is in the normal range.”
That is, they are a measurement of experienced, subtle cognitive functioning problems that occur in the absence of any visible signs of brain or psychological issues. To find out whether someone is experiencing Obj-SCD, researchers assess, among other factors, how efficiently that person can learn and retain new information.
Previous research has suggested that individuals with Obj-SCD are at a higher risk of mild cognitive impairment and forms of dementia.
In the current study, Prof. Bondi and the team found that beta-amyloid built up at a faster rate in the participants with Obj-SCD compared with those who were deemed cognitively healthy. Moreover, brain scans of people with Obj-SCD showed that these individuals experienced a thinning of brain matter in a region called the entorhinal cortex.
Past research has shown that the entorhinal cortex decreases in volume in people with Alzheimer’s disease. This is significant because this brain region plays a role in memory and spatial orientation.
The researchers also found that while people with mild cognitive impairment had higher quantities of beta-amyloid in their brains at the beginning of the study, this protein did not seem to build up any faster in these participants than it did in cognitively healthy individuals.
But why do the current findings potentially contradict a decades-old hypothesis about the development of Alzheimer’s? Prof. Bondi explains:
“This work […] suggests that cognitive changes may be occurring before significant levels of amyloid have accumulated. It seems like we may need to focus on treatment targets of pathologies other than amyloid, such as tau, that are more highly associated with the thinking and memory difficulties that impact people’s lives.”
“While the emergence of biomarkers of Alzheimer’s disease has revolutionized research and our understanding of how the disease progresses, many of these biomarkers continue to be highly expensive, inaccessible for clinical use, or not available to those with certain medical conditions,” adds first author Kelsey Thomas, Ph.D.
The new study’s findings could help change that by refocusing the research approach on more subtle markers of Alzheimer’s, such as those assessing for Obj-SCD.
“A method of identifying individuals at risk for progression to [Alzheimer’s disease] using neuropsychological measures has the potential to improve early detection in those who may otherwise not be eligible for more expensive or invasive screening,” says Thomas.
The maddening saga of how an Alzheimer’s ‘cabal’ thwarted progress toward a cure for decades
By Sharon Begley
June, 25, 2019
In the 30 years that biomedical researchers have worked determinedly to find a cure for Alzheimer’s disease, their counterparts have developed drugs that helped cut deaths from cardiovascular disease by more than half, and cancer drugs able to eliminate tumors that had been insurable. But for Alzheimer’s, not only is their no cure, there is not even a disease-slowing treatment. (See link for article)
Alzheimer’s has had a Cabal similarly to Lyme in that research has been hijacked by a group of individuals with blinders on. According to Norins, the 2017 Alzheimer’s Association had a conference in London where researchers from 70 countries could share progress. A keyword index of the presentations showed the largest entries, 110, were for amyloid/APP.The next most common item was tau, the tangled protein, with 85 entries. Inflammation—the body’s reaction to something—had 45 mentions. Presentations of germ importance had only single digit presence: prion proteins (8 entries), infectious disease (4 entries), bacteria (1 entry). Virus was not even listed as a keyword.