Archive for the ‘Alzheimer’s’ Category

Infectious Agents and Alzheimer’s Disease

https://www.imrpress.com/journal/JIN/21/2/10.31083/j.jin2102073

Infectious agents and Alzheimer’s disease

Thomas Piekut1, Mikołaj Hurła1, Natalia Banaszek1, Paulina Szejn1, Jolanta Dorszewska1,*, Wojciech Kozubski2, Michał Prendecki1
Show More
 
*Correspondence: dorszewskaj@yahoo.com; jolanta.dorszewska@ump.edu.pl (Jolanta Dorszewska)
Academic Editor: Rafael Franco
J. Integr. Neurosci. 2022, 21(2), 73; https://doi.org/10.31083/j.jin2102073
 
Submitted: 8 March 2021 | Revised: 25 March 2021 | Accepted: 29 April 2021 | Published: 28 March 2022
 
Abstract

Alzheimer’s disease (AD) is the leading cause of dementia worldwide. Individuals affected by the disease gradually lose their capacity for abstract thinking, understanding, communication and memory. As populations age, declining cognitive abilities will represent an increasing global health concern. While AD was first described over a century ago, its pathogenesis remains to be fully elucidated. It is believed that cognitive decline in AD is caused by a progressive loss of neurons and synapses that lead to reduced neural plasticity. AD is a multifactorial disease affected by genetic and environmental factors. The molecular hallmarks of AD include formation of extracellular amyloid (A) aggregates, neurofibrillary tangles of hyperphosphorylated tau protein, excessive oxidative damage, an imbalance of biothiols, dysregulated methylation, and a disproportionate inflammatory response.

Recent reports have shown that viruses (e.g., Herpes simplex type 1, 2, 6A/B; human cytomegalovirus, Epstein-Barr virus, hepatitis C virus, influenza virus, and severe acute respiratory syndrome coronavirus 2, SARS-CoV-2), bacteria (e.g., Treponema pallidum, Borrelia burgdorferi, Chlamydia pneumoniae, Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, Fusobacterium nucleatum, Aggregatibacter actinomycetemcmitans, Eikenella corrodens, Treponema denticola, and Helicobacter pylori), as well as eukaryotic unicellular parasites (e.g., Toxoplasma gondii) may factor into cognitive decline within the context of AD. Microorganisms may trigger pathological changes in the brain that resemble and/or induce accumulation of Apeptides and promote tau hyperphosphorylation. Further, the mere presence of infectious agents is suspected to induce both local and systemic inflammatory responses promoting cellular damage and neuronal loss.

Here we review the influence of infectious agents on the development of AD to inspire new research in dementia based on these pathogens.

_________________

For more:

Category:

Alzheimer's, Lyme, Parasites, research, Viruses

7 Conditions Masquerading As Dementia

https://greenmedinfo.com/blog/7-conditions-masquerading-dementia

7 Conditions Masquerading As Dementia

Monday, May 30th 2022
Written By:GMI Reporter

7 Conditions Masquerading As Dementia

More than 40% of dementia diagnoses have been shown to be wrong.  Here’s what may really be going on.  

Imagine this nightmare. For the last few years your mother has had serious memory problems.  She gets lost driving.  She repeats the same question to you over and over again.  She can’t process new information.  She loses her train of thought in mid-sentence.  A CT scan comes back with a diagnosis of early Alzheimer’s disease.  The doctors offer a prescription with little encouragement it will work.

Do you despair?

A new program from UCLA and the Buck Institute for Research on Aging offers new hope.  In the first study of its kind, researchers have proved that natural therapies can not only slow the progress of dementia but can actually reverse it.

In a paper titled “Reversal of Cognitive Decline: A novel therapeutic program” Dr. Dale Bredesen showed how 9 out of the 10 subjects diagnosed with dementia got their minds back.[i]

(See link for article)

______________________

SUMMARY:

  • Study results were remarkable with 9 of the 10 showing improvement in memory within three to six months.
  • Treatment was a “systems approach” which included dietary changes, exercise, brain stimulation, sleep optimization, pharmaceuticals and vitamins, etc.  Specifically:
    • eliminating all simple carbohydrates;
    • eliminating gluten and processed food;
    • increasing vegetables, fruits, and non-farmed fish;
    • reducing stress with yoga and meditation;
    • taking melatonin each night;
    • increasing sleep from 4-5 hours per night to 7-8 hours per night;
    • taking methylcobalamin (vitamin B12), vitamin D, CoQ10, and fish oil each day;
    • optimizing oral hygiene using an electric flosser and electric toothbrush;
    • hormone replacement therapy;
    • fasting for a minimum of 12 hours between dinner and breakfast;
    • fasting for a minimum of three hours between dinner and bedtime;
    • exercising for a minimum of 30 minutes, 4-6 days per week.
  • The only side effect was improved health and weight
  • (www.sharpagain.org) educates the public and the medical community about the reversible causes of dementia.
They give 7 areas to investigate before accepting a dementia or Alzheimer’s diagnosis.
  1. Nutritional imbalances and deficiencies. Deficiencies of omega 3s, vitamin B12, vitamin C, magnesium, selenium, probiotics, and other nutrients frequently cause symptoms of Alzheimer’s and dementia.
  2. Artificial food colors, flavors, and sweeteners. Artificial additives of all kinds may cause dementia symptoms.
  3. Prescription medication side effects. Drugs, especially pain medications, and psychotropic drugs can severely disrupt cognition.
  4. Inflammation from low-level infections, mold, food allergies, and Lyme Disease. Inflammation is the body’s attempt to get rid of a toxic element or organism, and so it occurs in many different situations, even root canals and urinary tract infections.
  5. Stress and stagnation/inactivity. Stress elevates cortisol levels, leading to inflammation, and in turn to hormone imbalances, cognitive impairment, heightened blood sugar levels, hypertension, delayed healing time, and susceptibility to disease.
  6. Thyroid and other hormonal imbalances. Many people diagnosed with Alzheimer’s or dementia simply have low levels of T3 thyroid hormone. However, standard thyroid tests completely miss T3 levels, and Synthroid (T4) doesn’t help. It is estimated that 10 to 15% of all nursing home residents may be there because of low T3.
  7. Mercury and other heavy metal poisoning. So-called silver amalgam fillings contain 50 percent mercury, and that mercury is neither stable nor inert. It off-gasses, crosses the blood-brain barrier, and destroys neurons even without contact. Removing these fillings is hazardous unless done with mercury-safe protocols.  Annual flu shots are another source of these toxins.

Since doctors are not experts in dementia causes or how to treat it, Sharp Again Naturally is building a medical advisory board and a database. It also offers help finding functional medicine specialists, naturopaths, or doctors who practice integrative medicine who are familiar with these areas.

Click here for more information on natural approaches to preventing and overcoming dementia.

Additional References

[i] Dale E. Bredesen, “Reversal of Cognitive decline: A novel therapeutic program.” AGING, September 2014, Vol. 6, No. 9.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.
© [5/30/22] GreenMedInfo LLC. This work is reproduced and distributed with the permission of GreenMedInfo LLC. Want to learn more from GreenMedInfo? Sign up for the newsletter here //www.greenmedinfo.com/greenmed/newsletter.

Category:

Alzheimer's, diet and nutrition, Lyme, Mold, research, Sleep, Supplements, Treatment, vaccines

Tulane Researcher Asks, “Could Chronic Lyme Contribute to Alzheimer’s Dementia?”

https://www.lymedisease.org/embers-lyme-alzheimers-dementia/

LymeDisease.org avatar
Focus – Opinions and Features
LymeDisease.org
15 APR 2022

Tulane researcher asks, “Could chronic Lyme contribute to Alzheimer’s dementia?”

By Kris Newby, Invisible International

In 2019, the late-great-science-writer Sharon Begley wrote an insightful article, “The maddening saga of how an Alzheimer’s ‘cabal’ thwarted progress toward a cure for decades.”

Begley’s reporting described how a powerful group of researchers became fixated on one theory of Alzheimer’s causation at the expense of all others.

Their hypothesis: that Alzheimer’s cognitive decline was caused by neuron-killing, beta-amyloid protein clumps in the brain, and that if you dissolved the clumps, the disease process would stop.

As this theory hit a brick wall, Begley showed how the actions of the cabal harmed patients: “…for decades, believers in the dominant hypothesis suppressed research on alternative ideas: They influenced what studies got published in top journals, which scientists got funded, who got tenure, and who got speaking slots at reputation-buffing scientific conferences.”

Decades later, with no cure or effective drugs for Alzheimer’s dementia, some researchers are gathering evidence on a different causation theory — that dementia could be triggered by any number of chronic infectious diseases, and that amyloid plaques are a byproduct of an active infection, not the cause.

One of these researchers is Monica Embers, PhD, an associate professor of microbiology and immunology at the Tulane National Primate Research Center. She’s also the leading expert in identifying treatments that can eradicate Lyme bacteria infections in nonhuman primates, our closest mammalian relatives.

CME course on infection and dementia

In her new continuing medical education course, “Chronic Infection and the Etiology of Dementia,” she lays out the evidence that the Lyme bacteria could be one possible cause of dementia.

Her theory is this: When pathogens like the Lyme bacteria sneak past the blood-brain barrier, the immune system doesn’t allow protective killer cells from the entering the inflexible brain cavity, because resulting brain inflammation and swelling could lead to death.

Instead, it encapsulates invading microbes with protein clumps, called beta-amyloid plaques or Lewy bodies, to stop the infection. As a person ages, the bodily processes that clean up this “brain gunk” slows, resulting in protein accumulation that impedes brain signaling and kills neurons.

In her 31-minute course, Dr. Embers describes the clinical symptoms of Alzheimer’s and Lewy body dementia, the impact on public health, genetic risks, and the list of infections associated with dementia-like symptoms.

The course also reviews a well-documented case study about a 54-year-old woman who was treated for the Lyme bacteria (Borrelia burgdorferi), developed dementia, then died 15 years after the initial infection. After death, B. burgdorferi was identified by PCR (DNA detection) in her brain and central nervous system (CNS) tissues, and by immunofluorescent staining of the bacteria in the spinal cord. (For more, read this peer-reviewed study.)

Dr. Embers and her study’s co-authors conclude, “These studies offer proof of the principle that persistent infection with the Lyme disease spirochete may have lingering consequences on the CNS. Published in postmortem brain autopsy images and extensive pathology tests are a compelling reason to pursue this line of scientific inquiry.”

You can watch this free CME course here.

Kris Newby is Communications Director of Invisible International, a 501(c)(3) nonprofit foundation dedicated to reducing suffering from invisible illnesses. The organization offers 24 free, online Continuing Medical Education (CME) courses on the diagnostics, epidemiology, immunology, symptoms, and treatment of Lyme disease, bartonellosis, and other vector-borne infections. 

For more:

Category:

Alzheimer's, Lyme, Psychological Aspects, research

Case Study: Autopsy Results on Alzheimer’s Death Showed Chronic Brain Infection

https://web.archive.org/web/20210615055543id_/https://scivisionpub.com/pdfs/borrelia-invasion-of-brain-pyramidal-neurons-and-biofilm-borrelia-plaques-in-neuroborreliosis-dementia-with-alzheimers-phenotype-1564.pdf

Borrelia Invasion of Brain Pyramidal Neurons and Biofilm Borrelia Plaques in  Neuroborreliosis Dementia with Alzheimer’s Phenotype 

Alan B. MacDonald* 

Received 29 Janaury 2021; Accepted: 25 February 2021

ABSTRACT 

Dementia in Lyme borreliosis complex has been reported, mainly in post-mortem studies without available  antemortem evidence of active borrelia infection. Blanc in 2014 studied living patients with Lyme neuroborreliosis dementia and several dementia phenotype illnesses including an Alzheimer’s Phenotype. Herein we report an additional case study of a longitudinal evolution of European neuroborreliosis over eight years from tick bite to mild cognitive disease, to advanced dementia to death with a brain Alzheimer’s disease phenotype and concurrent borrelia deposits in brain Alzheimer’s disease sites at autopsy. 

Intrathecal borrelia specific antibodies were detected by commercial diagnostic laboratories (antemortem).  Molecular autopsy tissue imaging was completed with borrelia specific DNA probes and an immunomicroscopic  detection histopathology method. 

Results: Autopsy showed intact spirochetes, fragmented spirochetes, deposits of borrelia-specific proteins inside  plaque lesions and inside of neurons, and borrelia DNA deposits in plaque and neuronal sites. Pure Alzheimer’s  disease (without Lewy bodies) was a routine neuropathological finding. 

CSF evidence for a brain compartment immune response is established here. Intrathecal antibodies to infection  presented as oligoclonal total CSF IgG bands (n=twelve increase to n=13 bands) and separate borrelia IgG  western blot band analysis in cerebrospinal fluids (seven diagnostic borrelia CSF antibody bands). Blood western  blot disclosed triple borrelia species infection; burgdorferi European type (eighteen bands), garinii (twelve bands)  and afzelii (eighteen bands). Total borrelia IgG antibodies in blood during life were two hundred-fold higher  than normal range. Western blot of cerebrospinal fluid prior to death disclosed 7 protein bands which were not  represented in simultaneous blood western blot studies, further validating the intrathecal fingerprint of a separate  brain compartment immune response to neuroborreliosis infection. 

Conclusion: Borrelia protein antigenic stimulation of intrathecal borrelia antibodies was caused by resident  deposits of spirochetal protein deposits in plaques, in diseased neurons, and in neuropil brain sites, and in intact brain spirochetes. Deposits of borrelia proteins inside neurons and brain phagocytes and in neuropil sites (invasosomes) confirm remnants of chronic brain infection. 

For more:

Category:

Alzheimer's, Lyme, research

Case Review: 80 Year Old With Lyme Encephalopathy Instead of Dementia

https://danielcameronmd.com/case-review-80-year-old-lyme-encephalopathy-instead-dementia/

Case review: 80-year-old with Lyme encephalopathy instead of dementia

lyme-encephalopathy

“An 80-year-old patient was admitted to the hospital after a fall, and subsequently developed an acute confused state requiring transfer to a neuropsychiatric unit,” writes Karrasch and colleagues in the journal Ticks and Tick-borne Diseases. [1]

By

“While mostly vigilant and awake, he intermittently lacked full orientation, had reduced attention, concentration, short-term memory function, increased motor activity, mild formal thought disorder (incl. some tangential thinking), but no frank psychotic symptoms,” the authors explain.

The man was diagnosed with delirium, potentially related to dementia. An abnormal F18-FDG-PET scan was interpreted as consistent with early Alzheimer’s disease. And memantine was prescribed.

However, the patient remained confused, despite receiving the antipsychotic medication risperidon and pipamperone for sleep disturbances. “The patient lacked orientation, had recurrent pervasive disturbances of sleep-wake-cycles, was intermittently restless, and also incontinent,” states Karrasch.

The patient’s spinal tap revealed an increased protein, lymphocytic pleocytosis of 260 leucocytes/μl, intrathecal IgM-synthesis, and elevated lactate. “The lymphocytic pleocytosis with signs of activation together with the dominance of intrathecal IgM-synthesis raised the differential diagnosis of neuroborreliosis,” writes Karrasch.

He also had an elevation of the chemokine CXCL13. And while this is not yet validated as a routine diagnostic tool, CSF [cerebrospinal fluid] CXCL13 may be another option to increase sensitivity and accuracy in diagnosing Neuroborreliosis, next to CSF lymphocytic pleocytosis, explains Karrasch.

The patient was given a 21-day course of ceftriaxone. As a result, his confusion and delirious symptoms resolved.

The man was “dismissed from the hospital in a clearly improved clinical status,” writes Karrasch, “despite an additional complication of aspiration pneumonia.”

The authors point out their case report demonstrates the possibility that confusion or acute encephalopathy can be a presenting feature of neuroborreliosis and that CXCL13 may be useful as a biomarker in central nervous system manifestations of Lyme borreliosis.

It is fortunate the doctors were able to recognize neuroborreliosis and successfully treat the 80-year-old man, or he might have been misdiagnosed with dementia.

References:
  1. Matthias Karrasch, Volker Fingerle, Katharina Boden, Andreas Darr, Michael Baier, Eberhard Straube, Igor Nenadic, Neuroborreliosis and acute encephalopathy: The use of CXCL13 as a biomarker in CNS manifestations of Lyme borreliosis, Ticks and Tick-borne Diseases, Volume 9, Issue 2, 2018, Pages 415-417, ISSN 1877-959X, https://doi.org/10.1016/j.ttbdis.2017.12.008.

___________________

**Comment**

It is highly likely this man will relapse and need further treatment; however, this topic is purposely avoided by the ‘powers that be’ as that would put direct salvos through their accepted narrative that a few weeks of antibiotics cures this.

How many more are walking around diagnosed with dementia, Alzheimer’s, MS, and other neurological labels when they have undiagnosed Lyme/MSIDS?

For more:

Category:

Alzheimer's, Lyme, research