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OTHER NEW ARTICLES AVAILABLE
https://soundofstars.org/newarticles.htm
PREFACE :
This document outlines key considerations for
the
three main health issues of
;
ALS –
LOU GEHRIGS DISEASE
DEMENTIA
/ ALZHEIMERS
STROKE
LIKE INCIDENT
Includes citations, white papers, references
Administrative
policy, current medical dogma and the narrative
provided
to the general public point to a “no hope” for
recovery,
specifically
for ALS.
Likewise per above, the outlook is similar for dementia and stroke.
Doctors
of distinction with a focus on healing and concerned not
only
with administrative policies know that in the real world actual
answers
are found.
Not
surprisingly, it turns out that not only are there a
significant
number
of Cases of recovery from ALS and dementia ‘ alzheimers
but
a number of existing Protocols and methods exist that
deserve
investigation
and consideration.
Recent
and current mainstream, conventional, recognized and peer
reviewed
Sources point to these as well as shedding light on what
the
actual causes Are likely to be.
Associated
with the hard copy of this document is also provided a
USB
data Thumb drive with this document contained with active
hyper links and Data files.
TABLE OF CONTENTS
ALS RECOVERIES & METHODS
FOR RECOVERY
EVIDENCE FOR FUNGUS AND FUNGAL TOXINS
METHODS -
ALZHEIMERS & DEMENTIA
METHODS – STROKE & STROKE LIKE
INCIDENTS
ALS RECOVERIES – NUMEROUS REAL WORLD EXAMPLES
As of July 2020,
Dr Bedlack had found 48
confirmed ALS reversals around the world.
All of these cases have been entered onto a database
to compare demographics, disease characteristics, other medical conditions, and
any treatments to people with ALS on other national registries.
This has uncovered some interesting similarities
between ALS reversals:
·
ALS reversals are more likely to me male
·
They experienced faster progression before they started to improve
·
They are more likely to have been using alternative therapies
How might these reversals be explained?
Dr Bedlack proposes
three possible explanations:
Misdiagnosis
The person never had ALS but something that
looks so like it, it was mistaken for ALS.
Alternative treatments
Did some of the treatments or therapies the ALS
reversals undertake actually work? This refers to
unprescribed and alternative treatments, either taken on their own, with other
compounds or as part of a regime.
The most common therapy that ALS reversals had
in common (6/48) was curcumin (found in turmeric). We have previously talked
about Dr Bedlack’s curcumin trial, which is part of
his Replication of ALS Reversals (R.O.A.R.) programme,
in which he will be giving 100 participants a type of curcumin called theracurmin, in the Winter 2020 edition of our members
magazine Thumbprint. The theracurmin trial is now
recruiting in the USA with results expected in 2021.
https://mndresearch.blog/2020/09/30/als-reversals-do-they-exist/
The man who beat Lou Gehrig’s disease
Healing
of Amyotrophic Lateral Sclerosis: A Case Report
|
Mangelsdorf I.a · Walach H.b · Mutter J.c, d Keywords: Amyotrophic lateral sclerosisProgressive muscular atrophyMotor neuron diseaseChelation therapyMercuryHeavy metals |
Complement
Med Res 2017;24:175-181
https://doi.org/10.1159/000477397
Once per week the patient received an
intravenous (i.v.) infusion of α-lipoic acid (600-1,200
mg), followed by sodium 2,3-dimercaptopropanesulfate (DMPS; 250 mg), together
with potassium (6 mmol), magnesium (12 mmol), calcium (200 mg), and glutathione
(GSH; 1,800 mg). Finally, after the DMPS infusion, sodium selenite (10-20 ml,
50 µg Se/ml) was i.v. injected separately. In
addition to the i.v. infusion, DMPS (250 mg) was
applied subcutaneously (s.c.) once per week. The
treatment frequency was gradually reduced during therapy, resulting in 45 s.c. and 30 i.v. applications
from March 26, 2013 until June 3, 2015. Until February
2, 2016, DMPS was applied orally 11 times (1 vial with 250 mg DMPS, mixed with
3 organic egg yolks, producing highly absorbable liposomal DMPS). Thus,
overall, the patient received 86 DMPS applications.
Daily dosages of orally applied vitamins,
micronutrients, and other supplements
In addition, the patient was advised to keep a
vegetarian diet with a high proportion of raw, unprocessed food (60-70% of
daily intake), also including wild herbs, and to reduce carbohydrate and
especially gluten intake.
The patient's compliance with this therapy has
been excellent. Motivated by the continuous improvement of his health, he has
been following the instructions up to now.
https://www.karger.com/Article/Fulltext/477397
https://www.karger.com/WebMaterial/ShowPic/858578
ALS Reversals: What Are They and How Can We Make
Them Happen More Often?
In addition to energy healing, some of the other
treatments associated with ALS reversals include Lunasin,
Protandim, Aimspro, and
bone marrow-derived stem cells through Brainstorm Cell, and embryonic stem
cells through Neuraltus. There will be several
novel patient-centric features of the trials in this ROAR Program, including:
https://www.als.org/blog/als-reversals-what-are-they-and-how-can-we-make-them-happen-more-often
How
to Deal With ALS (Lou Gehrig’s Disease)
KEY
POINTS :
In
2007, Columbia University researchers discovered that one aantibiotic
actually accelerated ALS deterioration by 25%
https://knowthecause.com/how-to-deal-with-als-lou-gehrig-s-disease/
Fungus used in traditional medicine could slow neuron loss in
ALS
Hirsutella sinensis (HS), a Chinese caterpillar fungus
that is used in traditional Chinese medicine has been found to minimize motor
neuron loss in mice models of amyotrophic lateral sclerosis (ALS). The fungus
was also found to extend the lifespan of mice, marking a promising development
in discovering therapeutic treatment for ALS.
The scientists investigated the effects of Hirustella
sinensis, a fungus that grows on insects, on ALS. A strictly regulated herbal remedy
for its high arsenic content when found in nature, HS is described as a “unique
fungus growing on caterpillars and is a highly valued tonic medicine claimed to
treat a wide range of disorders, such as asthma, chronic kidney disease, and
kidney transplant recipients,” in the study.
“Cordycepin (3’-deoxyadenosine), one of the major chemical
components of HS, has been identified to exert anti-oxidative,
anti-inflammation, antitumor, and neuroprotective effects,” the study
continues.
“Moreover, previous studies have further revealed a suppressive
role of cordycepin on […] microglia activation and inflammation in vitro.”
ELEVATED
TOXIC LEVELS OF GLUTAMATE ARE COMMON IN ALS CASES.
GLUTAMATE
IS PRODUCED BY FUNGUS AND ALS ASSOCIATED
BACTERIA
Fungus and bacteria cause glutamate elevation
SEE FUNGUS AS CAUSATION SECTION ;
The Deanna Protocol(R): Hope For ALS
and Other Neurological Conditions
Why
The Neuro-Health Protocol Works for ALS
Glutamate, ALS, and Cell Death:
To understand
the basis for the Neuro-Health Protocol, one must first consider the pathology
in neurodegenerative conditions in general and ALS specifically. Death of motor
neurons spreads throughout the body in individuals with ALS due to glutamate.
When cells die, they burst and release intracellular glutamate into the
extracellular space. This increase in extracellular glutamate causes
neighboring healthy motor neurons to die, to burst, and to release more
glutamate into extracellular space, which will kill even more neighboring
cells. This so-called storm of glutamate in ALS causes cell death to happen at
an exponential rate. (The spread of cell death via excess extracellular
glutamate has already been proven in other neurodegenerative conditions, such
as traumatic brain injury. It has not yet been proven in ALS research. However,
we know that all cells release glutamate when they die and that excess
extracellular glutamate kills neighboring cells, regardless of the
disease/condition.)
The same theory, hypothesizes that somehow, the exposure to
excess extracellular glutamate in ALS kills neighboring healthy neurons by
interrupting the Krebs Cycle in each of them. The Krebs Cycle interruption is
possibly a chief cause of cell death. After all, when cells cannot produce
energy efficiently, they die.
How the Neuro-Health Protocol by Simplesa®
May Help Stop Cell Death Caused by Extracellular Glutamate in ALS:
Does the
Neuro-Health Protocol neutralize the excess extracellular glutamate in ALS? No.
The Neuro-Health Protocol focuses on cell metabolism. The Neuro-Health Protocol
delivers Alpha-ketoglutarate (AKG) to the Krebs Cycle in the neurons. The
increase in AKG enables their mitochondria to produce enough energy to help
keep cells alive, despite their exposure to an unhealthy amount of
extracellular glutamate.*
Below is
a list of the substances other than AKG that comprise the Neuro-Health
Protocol, along with reasons why they are included.
GABA: PALS experience excitotoxicity. This causes uncontrollable
muscle twitching and makes it nearly impossible for their muscles to function
properly, even before those with ALS become paralyzed. GABA, an inhibitory
neurotransmitter, is used to reduce excitotoxicity. This in turn reduces
twitching, and enables those with ALS to maintain control of the muscles and limbs.*
CoQ10, Niacin, and 5HTP: These are the precursors to NADH. NADH is one of the
ingredients necessary for cells to produce the energy. We recommend that
individuals with ALS take these three substances, which will allow their bodies
to make NADH. (Taking NADH orally will not suffice because the body cannot
absorb it orally, which is why we recommend taking the precursors.)*
The Deanna Protocol(R) program was discovered
by Dr. Tedone, Deanna's father, only after failing,
again and again, with everything that he tried. The massage, non-exhausting
exercise and core supplements are inexpensive and available without
prescription from many suppliers. The program works for many ALS patients. It
is not a cure; however, it provides a better quality of life and has been shown
in ALS mice to extend life and improve motor skills. The rate of progression of
ALS symptoms reported in ALSFRS scores, is markedly reduced in those adhering
to the Deanna Protocol(R) program. There are few side effects reported, and
those are manageable for most, if the program is phased in, gradually, over
time. The main stream pharmaceutical giants and
neurologists have taken little notice or remain skeptical about any program
targeting metabolic support of motor neurons. However, we are winning over some
of the skeptics, when they see, first-hand, how much their own patients are
benefiting from the Deanna Protocol(R) program. An investigation at the
University of South Florida has shown that SOD1-G93A mice live longer and
better when on the core supplements of the Deanna Protocol(R) program. To our
knowledge, the Deanna Protocol(R) program is the only program tested on these particular mice that has ever shown a statistically
significant extension of life compared to controls. We were not surprised,
because the program already showed effectiveness in Deanna and many other
patients with ALS (PALS). More surprising to us is the anecdotal evidence that
the core supplements of the Deanna Protocol(R) program helps
patients with other neurological conditions, such as Alzheimer's. An
investigation of these other conditions is beyond our foundation's capability.
We don't have sufficient assets to meet the needs for research into ALS. Much
of the costs of the progress made to date have been borne by the Tedone's and a short list of donors to Winning the Fight,
Inc., a foundation established by the Tedone family.
If the foundation had more money, the research could progress much faster in
ALS and other neurological conditions could be included, which have shown
benefits to patients from taking the core supplements of the Deanna Protocol(R)
program. The authors are convinced that there is a common denominator among
many neurological conditions that could, potentially, benefit from the Deanna
Protocol(R) program or some program based on the core supplements of the Deanna
Protocol(R) program. Possibly, Alzheimer's, Parkinson's, stroke, traumatic
brain injury and other neurological conditions could all share a common pathway
for neuron cell death, a lack of energy in the cells. The authors believe that
one of the supplements taken as part of the Deanna Protocol(R) program provides
energy to distressed cells in which normal cellular metabolism has been
disrupted. From research completed after the manuscript for this book was
written, Dr. Tedone believes that many of these
neurological conditions could benefit from a program tailored toward keeping
more of the neurons from dying. This Preface and an Afterword have been added
to the soft cover edition of this book. If you are interested in our efforts to
discover a metabolic program for benefiting the health of patients with
neurological conditions resulting in neuron cell death, then turn to the
Afterword for a discussion on our evolving hypothesis.
https://www.simplesanutrition.com/why-the-neuro-health-protocol-works-for-als
Yeast model offers clues to possible drug targets for Lou
Gehrig's disease, study shows
https://www.sciencedaily.com/releases/2012/10/121028142318.htm
Scientists prevent neurodegeneration-associated protein clumping
in lab study
By artificially exposing FUS proteins to the natural process of
phosphorylation, researchers were able to prevent them from forming the harmful
clumps associated with ALS and frontotemporal dementia. In lab cultures of
human and yeast cells, the scientists stopped the harmful clumping of FUS
proteins by exposing them to phosphorylation, a process that makes precise
changes to the amino acid building blocks of proteins, increasing their
negative electric charge. The research shows that the increase in charge causes
the proteins to repel when they normally might aggregate.
The findings could eventually have positive implications for the
treatment of ALS — commonly called Lou Gehrig’s disease — and dementia.
https://www.brown.edu/news/2017-08-08/neurodegeneration
https://www.pnas.org/doi/10.1073/pnas.0401934101
METHODS
– ALS TREATMENTS
COPPER
ATSM AS A POTENTIAL TREATMENT FOR ALS
https://www.als.net/news/copper-atsm-as-a-potential-treatment-for-als
Cu-ATSM
https://www.caymanchem.com/product/17122
Targeting fungal menace through copper
nanoparticles and Tamrajal
Copper surfaces have been demonstrated to kill
vegetative as well as spores of different fungi such as C. albicans,
Aspergillus species etc.
https://www.sciencedirect.com/science/article/pii/S0975947617304813
METHODS – ALZHEIMERS & DEMENTIA TREATMENTS
A Bold New Experimental
Treatment for Alzheimer's Dementia
Ketone esters
prove astonishingly effective in a single case study.
Dr. Newport, sought a
different way to induce a higher level of ketosis in her husband. Using
coconut/MCT oil supplements in normal, healthy adults will raise ketone levels
in the blood from 0.09 mM to 0.3-0.4 mM immediately, and over time one can get
10 times those levels sticking to the supplement and a low carbohydrate diet.
Ingestion of 50 grams of a supplement called a ketone ester can double those
levels within an hour, leading to 6-7mM concentrations one can only find in
humans with prolonged fasting. Ingesting the supplement every 3-4 hours can
maintain these high levels.
After a few days of
escalating doses, Mr. Newport was brushing his own teeth, spontaneously dressing and bathing himself again, had improvements in
mood, and was able to recite the alphabet. After 6-8 weeks, his memory improved and he started to do yard work again. After 20
months, he maintained definite improvement, with his cognitive function seeming
to wax and wane with rising and falling ketone levels in his blood.
http://evolutionarypsychiatry.blogspot.com/2011/01/alzheimers-mild-cognitive-impairment.html
A ketone ester diet
exhibits anxiolytic and cognition-sparing properties, and lessens amyloid and
tau pathologies in a mouse model of Alzheimer's disease.Dec 29, 2012
https://www.nutreance.com/products/redimind
Ever wonder what it would
be like to
have something like
"rocket fuel" in your back pocket to give you that boost you need
during a long run or that fast group ride? Well....enter TdeltaS Ketones. TdeltaS
Ketones are the world’s first drinkable form of ketone ester, a sports drink
shown (via scientific data) to improve performance and recovery. So you are likely asking - what exactly is a ketone drink,
and why do I want it?
https://www.ebay.com/sch/i.html?_from=R40&_trksid=p2380057.m570.l1313&_nkw=keytone+ester&_sacat=0
Transcranial Pulse
Stimulation – A modern therapeutic procedure for treating Alzheimer’s dementia
A diagnosis of
Alzheimer’s brings many changes – both for those with the disease and for their
families. Acoustic pulses generated outside the body are introduced
specifically into the brain regions requiring treatment. e NEUROLITH®
therapy system and applies ultrasound gel to the scalp or hair. It is not
necessary to shave the patient’s head. The ultrasound gel is needed to ensure
optimal transmission of the pulses. The patient then puts on a pair of glasses
so that the position of the head can be detected. During the
course of the treatment, the therapist moves the handpiece gently over
the corresponding areas of the scalp and the skull. On a screen, both doctor
and patient can see exactly which area of the brain is currently being reached.
A therapy session
generally lasts about 30 minutes. Overall, a TPS® treatment series includes an
average of 6 sessions, all taking place within 2 weeks.
DEMENTIA
BLUE LIGHT THERAPY
Researchers
are focused on the potential cognitive
benefits of near-infrared light pulsed at 40 Hz. Current
research is based on the groundbreaking study by an MIT research lab in 2017 that found that mice bred to have Alzheimer’s had improved
cognition after being exposed to near-infrared light pulsed at 40 Hz. When the
mice were dissected, the amyloid plaques and tau deposits associated with
Alzheimer’s were significantly reduced.
A 2019 study found
that after one treatment with the Vielight Neuro
Gamma, there was an increase in gamma, alpha, and beta brain waves; these brain
waves are considered important in attention and cognition.
The
Neuro Gamma 3 may be effective for when a progressive, neurodegenerative
disease is suspected, such as possible CTE (and Alzheimer’s), and for older
people, such as 50 years of age or older. It may help younger people — see the
information below. Do
not use the Vielight Neuro Gamma 3 for those with a
history of PTSD or significant anxiety, as the 40 Hz pulse may
be overstimulating.
Vielight Neuro Gamma 3 in current
research
Vielight Neuro Gamma 3
Use promo code BRAINHEALTH10 for
10% off at
- The University of Utah TBI and Concussion Center,
Department of Neurology School of Medicine conducted a
study, using the Vielight Neuro Gamma, entitled Use of PBM to Improve Brain Health and Resiliency in
Individuals with Repetitive Head Hits: A Pilot Study.
They are currently compiling the results and will publish them next year. Read
about this study in our blog post.
- Researchers at the Boston VA Medical Center, and
Boston University School of Medicine, Neurology, conducted
recent case studies of light therapy that showed positive effects for
retired pro football players with neurodegenerative symptoms — the study
includes documentation of positive effects from Vielight
Neuro Gamma home use. Read about these case studies in our blog post.
- A former athlete in their 30s who had a history of
repetitive head impacts and debilitating symptoms had
significantly positive effects from using the Vielight
Neuro Gamma. The study was conducted by The University of California, San Francisco,
Departments of Radiology & Biomedical Imaging and Psychiatry &
Behavioral Science, and the San Francisco VA Health Care System.
The researchers who are planning a larger clinical trial. Read
about this study in our blog post.
- There is an ongoing clinical
trial at the
University of Toronto using the Vielight Neuro
Gamma for Alzheimer’s; read more about the clinical trial.
Previous small
clinical trials showed positive results for
Alzheimer’s patients.
Vielight Neuro Alpha 3 – pulsed at 10 Hz
Overview
Researchers
are recommending the Neuro Alpha 3 for those under age 50 and without suspected
progressive neurodegenerative disease. They recommend the Neuro Alpha 3 for
people with PTSD or significant anxiety, as it will not be overstimulating.
The positive
effects of near-infrared light (whether 10 Hz or 40 Hz) include increased cerebral blood flow,
increased (ATP) energy production, increased neuroprotection and brain repair, and
reduced inflammation.
Vielight Neuro Alpha 3
Use promo code BRAINHEALTH10 for
10% off at
Vielight Neuro Alpha 3 in current
research
- Vielight
Neuro Alpha for Alzheimer’s research
- The Boston VA Research Institute,
Inc. and the VA Boston Healthcare System are currently
running a study if light therapy can improve thinking and memory in
people who have suffered one or more mild-to-moderate traumatic brain
injuries (TBIs), including concussions and subconcussive
impacts. To learn about the study, including how to apply to enroll in
the study, please
read our blog post.
- A 2017 case series report found
the Vielight Neuro Alpha to have positive
effects on cognition in mild to moderately severe dementia cases.
- Vielight
Neuro Alpha use with veterans with chronic post-concussive symptoms
- A VA blog post, titled Gulf War Veteran says
his memory has improved and energy is up, discusses a program
that provides LED light therapy to veterans; the device being used is the
Vielight Neuro Alpha. The program is through
the Center for Compassionate Care Innovation and
the VA Boston Healthcare System, Rehabilitation Medicine Services, LED
TBI CLINIC.
https://www.concussionalliance.org/blog/2022/4/25/choosing-a-light-therapy-device-based-on-research
https://www.vielight.com/devices/
https://www.vielight.com/devices/vielight-neuro-alpha/
https://www.vielight.com/devices/vielight-neuro-gamma/
https://www.usailighting.com/research-led-light-therapy-alzheimers
https://cognitotx.com/platform
https://gammalighttherapy.com/
https://best-alzheimers-products.com/alternative-therapy-for-alzheimers/light-therapy-for-alzheimers
Galantamine
in Alzheimer's disease
How does galantamine
help Alzheimer's?
Galantamine is in a class
of medications called acetylcholinesterase inhibitors. It works by increasing
the amount of a certain natural substance in the brain that is needed for
memory and thought. Galantamine may improve the ability to think and
remember or slow the loss of these abilities in people who have AD.
Can galantamine worsen
dementia?
There is no evidence that
galantamine prevents Alzheimer's disease from getting worse.
https://pubmed.ncbi.nlm.nih.gov/18088197/
Huperzine A
Early studies suggest that huperzine
A might improve memory and protect nerve cells, which could slow the cognitive
decline associated with Alzheimer's.
Can huperzine A prevent memory loss and
improve cognitive function in people with Alzheimer's disease?
Answer From Brent A. Bauer, M.D.
Huperzine (HOOP-ur-zeen)
A, a dietary supplement derived from the Chinese club moss Huperzia
serrata, is sparking some interest as a potential treatment for Alzheimer's
disease.
Huperzine A acts as a cholinesterase inhibitor — a type of medication that
works by improving the levels of neurotransmitters in the brain. Small early
studies suggest that huperzine A might improve memory
and protect nerve cells, which could slow the cognitive decline associated with
Alzheimer's.
Some studies have found evidence that huperzine
A might significantly improve cognitive performance in people with Alzheimer's
disease. However, a recent systematic review found that the quality of the
evidence of huperzine A's effectiveness was low.
Another systematic review found that huperzine
A did have a beneficial effect on cognitive function. But,
the review noted that the results should be interpreted with caution because of
problems with the way the trials were conducted.
STROKE
RECOVERY
the
glymphatic system is affected in strokes and other neurological issues. See
this video for info on the glymphatic system. https://www.youtube.com/watch?v=ci5NMscKJws
Benefits
that may also be helpful for stroke as well based on experience as it appears
to increase strength and stamina. https://www.youtube.com/watch?v=OfA7Gkdas90
EVIDENCE FOR FUNGUS AND FUNGAL TOXINS
-
SIGNIFICANT CAUSATION FOR ALS
These fungal structures were present in all ALS
patients analyzed and the species present in the CNS were precisely identified by
NGS, rendering the genera Candida, Malassezia, Fusarium, Botrytis, Trichoderma,
and Cryptococcus as those most prominent in ALS patients.
https://www.frontiersin.org/articles/10.3389/fnins.2019.00171/full
ELEVATED
TOXIC LEVELS OF GLUTAMATE ARE COMMON IN ALS CASES.
GLUTAMATE
IS PRODUCED BY FUNGUS AND ALS ASSOCIATED
BACTERIA
SEE
FOLLOWING CITATIONS ;
Fungal Neurotoxins and Sporadic Amyotrophic Lateral Sclerosis
Exposure of neurons to
fungal neurotoxins elicits a significant increase in glutamate production. High
levels of glutamate stimulate TDP-43 translocation and modification, providing
a link between fungal infection and one of the molecular and histologic
hallmarks of sporadic ALS. A recent study provided evidence of a variety of
fungi in the cerebrospinal fluid and brain tissue of ALS patients. This review
provides a rational explanation for this observation. If a fungal infection
could be confirmed as a potential cause of ALS, this could provide a
straightforward treatment strategy for this fatal and incurable disease.
·
May 2019
·
Neurotoxicity Research 35(2)
Neurotoxicity Research volume 35, pages969–980
(2019)Cite this article
·
1019 Accesses
·
10 Citations
·
19 Altmetric
Abstract
We review several lines
of evidence that point to a potential fungal origin of sporadic amyotrophic
lateral sclerosis (ALS). ALS is the most common form of motor neuron disease
(MND) in adults. It is a progressive and fatal disease. Approximately 90% cases
of ALS are sporadic, and 5–10% are due to genetic mutations (familial). About
25 genes implicated in familial ALS have been identified so far, including SOD1
and TARDBP, the gene encoding 43 kDa transactive
response (TAR) DNA-binding protein (TDP-43). Despite intensive
research over many decades, the aetiology of sporadic
ALS is still unknown. An environmental cause, including grass or
soil-associated fungal infections, is suggested from a range of widely diverse
lines of evidence. Clusters of ALS have been reported in soccer players,
natives of Guam and farmers. Grass-associated fungi are known to produce a
range of neurotoxins and, in symbiotic associations, high levels of fungal
SOD1. Exposure of neurons to fungal neurotoxins elicits a significant
increase in glutamate production. High levels of glutamate stimulate TDP-43
translocation and modification, providing a link between fungal infection and
one of the molecular and histologic hallmarks of sporadic ALS. A recent study
provided evidence of a variety of fungi in the cerebrospinal fluid and brain
tissue of ALS patients. This review provides a rational explanation for this
observation. If a fungal infection could be confirmed as a potential cause of
ALS, this could provide a straightforward treatment strategy for this fatal and
incurable disease.
https://link.springer.com/article/10.1007/s12640-018-9980-5
Evidence for
Fungal Infection in Cerebrospinal Fluid and Brain Tissue from Patients with
Amyotrophic Lateral Sclerosis
Ruth Alonso1,
Diana Pisa1, Ana Isabel Marina1, Esperanza Morato1,
Alberto Rábano2, Izaskun Rodal2,
Luis Carrasco1 
1. Centro de Biología Molecular “Severo
Ochoa”. c/Nicolás Cabrera, 1. Universidad Autónoma de
Madrid. Cantoblanco. 28049 Madrid. Spain.
2. Department of Neuropathology and Tissue Bank, Unidad de Investigación
Proyecto Alzheimer, Fundación CIEN, Instituto de Salud
Carlos III, Madrid. Spain.
This is an open access article distributed under the terms of
the Creative
Commons Attribution (CC BY-NC) License. See http://ivyspring.com/terms for full terms and conditions.
Citation:
Alonso R, Pisa D, Marina AI, Morato E, Rábano A, Rodal I, Carrasco L.
Evidence for Fungal Infection in Cerebrospinal Fluid and Brain Tissue from
Patients with Amyotrophic Lateral Sclerosis. Int J Biol Sci 2015;
11(5):546-558. doi:10.7150/ijbs.11084. Available from https://www.ijbs.com/v11p0546.htm
https://www.ijbs.com/v11p0546.htm
Searching for Bacteria
in Neural Tissue From Amyotrophic Lateral Sclerosis
https://www.frontiersin.org/articles/10.3389/fnins.2019.00171/full
ALS Study Finds Bacteria, Fungi in Central Nervous System of ...
Bacteria and fungi were found in the central nervous systems of
ALS patients that might be related to the onset of disease,
a study reports.
... a group of researchers from the Universidad Autónoma de Madrid in Spain suggested that ALS might be
caused by a fungal infection, based on the observation of fungi structures on
tissue samples from patients and on the identification of several species of
fungi in the CNS (composed of the brain, brainstem and
cerebellum) of individuals with ALS.
They analyzed frozen CNS tissue samples from 11 patients diagnosed
with ALS. To detect the presence of bacteria, scientists isolated DNA from the
patients’ CNS samples and performed nested polymerase chain reaction (PCR) to
look for bacterial DNA. Next-generation sequencing (NGS) was then used to
identify which bacteria species were present in the samples.
Using this approach, the scientists found bacterial DNA in
different regions of the CNS in all tissue samples. In addition, with
immunohistochemistry (a technique that allows researchers to visualize
structures in great detail using specific antibodies),
they detected the presence of bacteria in neural tissue samples from patients,
which was consistent with their previous findings.
NGS confirmed the presence of bacterial DNA in all tissue samples.
Despite the large variability of bacteria orders found in the patients’
samples, the phyla Proteobacteria and Actinobacteria were the most represented
in all regions of the CNS.
“The confirmation that [ALS and other neurological] diseases are
caused by fungi or bacteria, or both, should come from clinical trials using
already approved antifungal and antibacterial agents. Patients with these
neurodegenerative diseases do not have to wait for the development of new
therapeutic agents. These studies using safe antimicrobial compounds could be
started immediately after approval of these trials,” they added.
fungal yeast and hyphal structures can be directly visualized in
neural tissue of ALS patients, and a number of fungal
species have been identified in the central nervous system (CNS). In the
present work, we tested the possibility that bacterial infections can accompany
these mycoses. Our findings establish the presence of bacterial DNA in
different regions of the CNS from all ALS patients examined. Specifically, we
used PCR and next generation sequencing (NGS) to precisely determine the
bacterial species present in ALS tissue. Consistent with these findings,
immunohistochemistry analysis of CNS sections using specific anti-bacterial
antibodies identified prokaryotic cells in neural tissue.
https://www.frontiersin.org/articles/10.3389/fnins.2019.00171/full
Bacteria and Fungi Found in
Central Nervous System of ALS Patients, Study Reports
ALS might be caused by a fungal infection,
based on the observation of fungi structures on tissue samples from patients
and on the identification of several species of fungi in the CNS (composed of
the brain, brainstem and cerebellum) of individuals
with ALS.
“The
confirmation that [ALS and other neurological] diseases are caused by fungi or
bacteria, or both, should come from clinical trials using already approved
antifungal and antibacterial agents. Patients with these neurodegenerative
diseases do not have to wait for the development of new therapeutic agents.
These studies using safe antimicrobial compounds could be started immediately
after approval of these trials,” they added.
https://alsnewstoday.com/news-posts/2019/03/20/bacteria-fungi-central-nervous-system-als-patients/
Searching for
Bacteria in Neural Tissue From Amyotrophic Lateral
Sclerosis
We recently advanced the idea
that ALS might be caused by fungal infection. Indeed, fungal yeast and hyphal
structures can be directly visualized in neural tissue of ALS patients, and a number of fungal species have been identified in the
central nervous system (CNS). In the present work, we tested the possibility
that bacterial infections can accompany these mycoses.
https://www.frontiersin.org/articles/10.3389/fnins.2019.00171/full
The most representative species was Cutibacterium
acnes (formerly known as Propionibacterium acnes)
Other species detected included Corynebacterium sp (patient ALS5, SC) (band size 630 bp), Fusobacterium nucleatum (ALS11, SC) (band size 460 bp), Lawsonella clevelandesis (ALS9,
SC) (band size 540 bp) and Streptococcus thermophilus (ALS8, MD) (band size
488bp).
Sequencing of the extracted DNA showed that the amplified product
corresponded to Burkholderia species
prokaryotic cells in neural tissue.
Proteobacteria and Actinobacteria
fungal yeast and hyphal structures
These fungal structures were present in all ALS
patients analyzed and the species present in the CNS were precisely identified
by NGS, rendering the genera Candida, Malassezia, Fusarium, Botrytis,
Trichoderma, and Cryptococcus as those most prominent in ALS patients.
https://www.frontiersin.org/articles/10.3389/fnins.2019.00171/full
Detection of Bacterial DNA From ALS Patients by NGS
The order Sphyngomonodales, the family Methilobacteriaceae
and the genus Cupriavidus seemed to be the most
prevalent bacterial groups in ALS patients.
The phyla Actinobacteria
and Proteobacteria were found in all three regions of the 11 ALS patients
analyzed. The phyla Firmicutes and Bacteriodetes were
also prevalent, whereas other phyla were less represented. For example,
Fusobacteria was found in only one patient, in all three CNS regions. In
addition, we detected a great variability in the bacterial orders present in
ALS patients. For instance, Actinomycetales, Burkholderiales and Rhizobiales
were detected in all ALS patients, whereas Xanthomonadales
was found only in two patients (ALS6, MD and ALS7, SC3). These findings reveal
the irregular range of bacteria in the different samples tested, indicating
that these bacteria are likely not due to contamination during DNA extraction
and NGS analysis.
the bacterial genera Acrobacter, Thermomonas, Hemophylus, Propionibacterium, and Corynebacterium are more
represented in MC, MD, and SC regions in ALS patients than in AD patients.
Further, Propionibacterium acnes is the most representative in each region with
respect to AD patients.
These
fungal structures were present in all ALS patients analyzed and the species
present in the CNS were precisely identified by NGS, rendering the genera
Candida, Malassezia, Fusarium, Botrytis, Trichoderma, and Cryptococcus as those
most prominent in ALS patients.
To complement the bacterial DNA study, we performed
immunohistochemistry to directly test for prokaryotic structures in the CNS of
ALS patients. Initially, we performed double immunofluorescence analysis using
two different antibodies: a mouse monoclonal antibody against bacterial
peptidoglycan (shown in green), and a rabbit polyclonal antibody against
Candida albicans (shown in red) (Figure 6). Several prokaryotic morphologies
could be detected in different CNS regions by confocal microscopy. For example,
a bacilliform structure of 4–7 μm in size was
recognized with the anti-peptidoglycan antibody (Figures 6V,X).
Smaller bacilli of 1–2 μm were also immunostained with this antibody in some sections (Figures
6B,G). These bacilli are clearly differentiated from
yeast-like structures that were recognized with the anti-C. albicans antibody
(see for instance Figure 6K). In addition to these prokaryotic morphologies, a
variety of immunopositive microbial structures were
detected, in good agreement with our recent study (Alonso et al., 2017b). Some
of these microbial cells were clearly intranuclear (Supplementary Figure 3).
Different bacilli-like morphologies that stained with the anti-peptidoglycan
antibody could also be clearly seen. The range in sizes of these structures
suggests that they represent different species. Moreover, yeast-like cells and
some hyphae were also evident. Most likely, the structures immunostained
with the anti-peptidoglycan antibody are prokaryotic in origin, although the
anti-C. albicans antibody not only cross-reacts with several fungal species,
but also with some bacteria (Pisa et al., 2017). Nevertheless, none of these
antibodies recognizes human cells.
We also immunostained the samples with a
rabbit polyclonal antibody against Chlamydophila pneumoniae (shown in green)
and with a rat polyclonal antibody raised against the fungus Trichoderma viride (shown in red) (Figure 7). It must be taken into
consideration that these two antibodies can cross-react with prokaryotic and
yeast-like cells (Pisa et al., 2017). Both the anti-C. pneumoniae antibody and
the anti-T. viride antibody recognize a variety of
bacteria and also immunoreact
with several yeast species. However, the spectrum of species recognized by both
antibodies is different. Notably, this double immunofluorescence analysis also
revealed a number of microbial structures (Figure 7).
In some instances, small rounded prokaryotic-like cells were evidenced (see
Figures 7C,P). On other occasions, larger rounded
cells or even elongated structures were detected (Figures 7A,B,J–M).
Detection of Corpora Amylacea by
Immunohistochemistry
Corpora amylacea (CA) are small (10–50 μm) basophilic bodies that have been identified in
several neurodegenerative diseases including AD and Parkinson’s disease (Pisa
et al., 2016a). By proteomic analysis, we recently demonstrated that in
addition to human proteins, CA purified from brain tissue of patients with AD
contain fungal and bacterial proteins (Pisa et al., 2018). We next examined for
CA in ALS patients, and whether they stained positive with anti-peptidoglycan
or anti-C. albicans antibodies. CA were found in several tissue sections from
different ALS patients, and a clear immunostaining with anti-peptidoglycan
antibodies (green) was observed in many of these CA (Figure 8). In some
instances, immunoreactivity of CA with a C. albicans antibody (red) was also
observed (Figures 8C,E,O). This result is consistent
with the concept that CA contain both fungal and bacterial macromolecules and
their function might be to collect the cellular and microbial debris provoked
by infections in the brain (Pisa et al., 2018). Since CA are generated over
long time periods (months or even years), these microbial proteins were likely
sequestered in CA when the patients were alive.
These fungal structures were present in all ALS
patients analyzed and the species present in the CNS were precisely identified
by NGS, rendering the genera Candida, Malassezia, Fusarium, Botrytis,
Trichoderma, and Cryptococcus as those most prominent in ALS patients.
https://www.frontiersin.org/articles/10.3389/fnins.2019.00171/full
Fungal-contaminated grass and well water and sporadic amyotrophic
lateral sclerosis
Peter William French, PhD,1* Russell Ian Ludowyke,2 and Gilles J. Guillemin3
Neural Regen Res. 2019 Sep; 14(9): 1490–1493.
PMCID: PMC6557101
PMID: 31089037
A wide variety of fungi have been reported in drinking water
including Acremonium, Alternaria, Aspergillus, Cladosporium, Fusarium,
Penicillium and Trichoderma. Some of these are known to produce neurotoxic
mycotoxins. Despite this, drinking water is not routinely monitored for fungal
contamination. Fungal contamination could explain the close correlation between
distribution of well water and cases of sporadic ALS in the United States.
Cyanobacteria are found in algal blooms in a variety of
freshwater, and marine habitats and produce several toxins that have adverse
effects on human health.
Schwartz and Klug (2016b) did not identify the agent in well water
that potentially induced ALS, but they proposed that it could be Legionella
bacteria.
Common filamentous fungi detected in drinking water include
Acremonium, Alternaria, Aspergillus, Cladosporium, Fusarium, Penicillium and
Trichoderma (Babič et al., 2017). As noted
above, some of these genera produce mycotoxins that are neurotoxic.
Fungal infections are usually chronic and progressive if
undetected and untreated. It is known that neurons respond to some fungal
neurotoxins by increasing glutamate production in vivo (Bradford et al., 1990).
Excessive glutamate secretion from neurons is one of the hallmarks of ALS and
has been linked to the destruction of motor neurons as a result
of excessive activation of glutamate receptors (Foran
and Trotti, 2009).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6557101/
Fungal Neurotoxins and Sporadic Amyotrophic Lateral Sclerosis
https://pubmed.ncbi.nlm.nih.gov/30515715/
https://www.research.va.gov/programs/tissue_banking/ALS/field-based-meeting2020/RichardBedlack.pdf
Evidence for Fungal Infection in Cerebrospinal Fluid and Brain
Tissue from Patients with Amyotrophic Lateral Sclerosis
https://www.ijbs.com/v11p0546.htm
Fungus used in traditional medicine could slow neuron loss in ALS
ALS, UNTREATED BABESIA, UNTREATED BARTONELLA, UNTREATED LYME,
ETC. IS GENETIC ALS VULNERABILITY
INITIATED BY INFECTIONS?
Charles decided to treat his ALS with a combination of antibiotics
(ceftriaxone, Flagyl, azithromycin) and anti-protozoals
(Mepron and Malarone). His
rationale for using them is based on proposed link between ALS and some
infections, such as Babesia and Untreated Lyme Disease.
B. burgdorferi (Bb), the spirochete bacteria that causes Lyme
disease.
Further, during a visual scan of his blood, rings around his red
blood cells were also detected, indicating a probable co-infection with
Babesia, malaria-like protozoa that are estimated to be transmitted in over 60%
of Lyme infections.
Direct and indirect testing for Bartonella, the immune suppressing
emerging infection carried by more vectors than any infection in the world [per
Edward B. Breitschwerdt, DVM. Professor of Medicine
and Infectious Diseases] is not known to have been performed or at what level
of sophistication.
https://www.personalconsult.com/posts/als-and-untreated-babesia-lyme-and-bartonella.html
Immunohistochemistry Analysis
The antifungal antibodies employed have been described previously
(Pisa et al., 2015, 2016a). The following bacterial antibodies were used:
rabbit polyclonal antibody against Chlamydophila pneumoniae, which immunoreacts with the major outer porin (Biorbyt, Cambridge, United Kingdom), used at 1:20 dilution;
and mouse monoclonal antibody against peptidoglycan (Thermo
Fisher Scientific, Waltham, MA, United States), used at 1:20 dilution. Standard
techniques were used for paraffin embedding and sectioning of CNS tissue.
Protocols for immunohistochemical analysis have been described (Pisa et al.,
2016b). Most of the images were obtained with a Zeiss LSM710 multiphoton
confocal laser scanning microscope equipped with the upright AxioImager.M2
stand (Zeiss), running ZEN 2010 software. Images were deconvoluted using
Huygens software (4.2.2 p0) and visualized with ImageJ (NIH).
https://www.frontiersin.org/articles/10.3389/fnins.2019.00171/full
Institute of Neurological Recovery
Stroke & Brain Injury Recovery.
METHOD
– STROKE "Brain
Stroke Aneurysm Infarction relief via Etanercept Enbrel"
Stroke
victims are known to recover well and rapidly via the trial drug etanercept
Reverse Stroke | 60 Minutes
https://www.youtube.com/watch?v=-nEtQ-Wxkas
4.78M subscribers
About the Institute
Edward Tobinick, M.D., the founder and
Director of the Institute of Neurological Recovery, invented the remarkable
breakthrough perispinal etanercept treatment for
stroke and chronic brain injury, first used in 2010, now, in 2022, with
thousands of patients treated from 91 countries.
In October 2018, the
Australian Government announced their designation of substantial funding to
study perispinal etanercept(PSE)
for treatment of stroke. On January 3, 2020 a
university, double-blind, randomized, placebo-controlled, clinical trial
confirmed the efficacy of perispinal etanercept for
treatment of chronic, post-stroke pain. Dr. Tobinick
was instrumental in the design of the university study.
The INR accepts patients
for treatment from all parts of the world, and has
treated patients from every populated continent of the world.
Scientific articles from
hundreds of academic scientists around the world have cited INR publications.
https://www.facebook.com/InstituteOfNeurologicalRecovery/videos/1460865233951848/
Summary
Etanercept
is a protein therapy based on the binding fragment of the tumour
necrosis factor alpha receptor used to treat severe rheumatoid arthritis and
moderate to severe plaque psoriasis. It consists of 934 amino acids. It is used
to treat or manage a variety of inflammatory conditions including rheumatoid
arthritis (RA), ankylosing spondylitis (AS), and juvenile idiopathic
poly-articular arthritis (JIA).
https://go.drugbank.com/drugs/DB00005
https://www.sciencedirect.com/science/a
... 2X1552650X
Chemical
and physical data
Formula
C2224H3475N621O698S36
Molar
mass 51235.07 g·mol−1
https://en.wikipedia.org/wiki/Etanercept
============
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