An Association of Pathogens and Biofilms with Alzheimer’s Disease, 2021

Abstract

As one of the leading causes of dementia, Alzheimer’s disease (AD) is a condition in which individuals experience progressive cognitive decline. Although it is known that beta-amyloid (Aβ) deposits and neurofibrillary tangles (NFT) of tau fibrils are hallmark characteristics of AD, the exact causes of these pathologies are still mostly unknown. Evidence that infectious diseases may cause AD pathology has been accumulating for decades. The association between microbial pathogens and AD is widely studied, and there are noticeable correlations between some bacterial species and AD pathologies, especially spirochetes and some of the oral microbes. Borrelia burgdorferi has been seen to correlate with Aβ plaques and NFTs in infected cells. Because of the evidence of spirochetes in AD patients, Treponema pallidum and other oral treponemes are speculated to be a potential cause of AD. T. pallidum has been seen to form aggregates in the brain when the disease disseminates to the brain that closely resemble the Aβ plaques of AD patients. This review examines the evidence as to whether pathogens could be the cause of AD and its pathology. It offers novel speculations that treponemes may be able to induce or correlate with Alzheimer’s disease.

https://www.mdpi.com/2076-2607/10/1/56/htm

 

Drexel University. They've had Judith Miklossy speak at their conferences in the past, so they should have a good familiararity with spirochetal infections of the brain, in particular.

 

Isn't that what causes syphilis? I wouldn't imagine it's very common at all these days, unless they're on about a different type of infection.

 

Does anyone know if anyone tried targeting those pathogens and if it affected disease progression?

 

https://pubmed.ncbi.nlm.nih.gov/34585987/

"More than 75 species/species-level phylotypes belonging to the genus Treponema inhabit the human oral cavity. Treponema denticola is commonly associated with periodontal disease, but the etiological roles and ecological distributions of other oral treponemes remain more obscure."

WW2 saw huge levels of syphilis and in the UK for example didn't reach stable levels till the mid 50s so T. pallidum might have a large impact in older populations. Syphilis is still a major public health problem: https://www.gov.uk/government/publications/tracking-the-syphilis-epidemic-in-england

"Cases of syphilis in England have increased considerably in recent years: 2019 was the year with the highest number of diagnoses since the 1940s, with a 10% increase compared to 2018"

 

I watched a program in 2003 where a Canadian doctor said that they found Chlamydia Pneumoniae in autopsied brains of AD patients and that it really shouldn't be there. He explained that treating some patients with AD (early) with antibiotics and anti inflammatory meds prevented/slowed the progression.

 

My Mother's cognitive impairment developed very quickly after a kidney infection. She was never the same after she had it removed. Some doctors said she had AD while a few others said they didn't know or didn't think she did.

 

I think an Alzheimer's Genome-wide association studies (GWAS) study indicated that the disease was infectious. However, it's taken time to understand the mechanism - possibly an indication of the value of GWAS and an indication that it can take time to understand [EDIT - a disease i.e. after a GWAS study provides clues]. Also, Alzheimer's research should be well funded, i.e. considering the societal costs, yet it hasn't been.

@Simon M

 

Reminds me of a famous Scottish climber Hamish MacInnes who developed an infection and was sectioned - form of dementia. He recovered and gradually rebuilt (some of) his memory.

 

Did anyone notice the reference to Q fever?

Q fever can result in a post infectious disabling fatigue which looks like ME/CFS.

 

Do we know whether infections are causative or increases the risk of developing AD?

There are many inconsistencies in the literature.

 

Just Googled for a few minutes and came up with this:
"GWAS now implicates innate immune genes (44, 51) as being a risk factor and supports a primary role for the inflammatory elements of AD pathology via inappropriate activation of the complement system (5254) in association with Ab plaques and NFTs (55)."
"Recently, genetic overlap between AD, C-reactive protein (CRP) and plasma lipids was demonstrated by using summary statistics from GWAS of over 200,000 individuals (183). There may also be interplay between genetic risk and environmental risk factors such as toxins and or bacterial, viral and fungal pathogens in LOAD reflecting its complex and multifactorial etiology (1)"
[https://www.tandfonline.com/doi/pdf/10.3402/jom.v7.29143]

I recall a GWAS study which identified a gene which increased/decreased the risk of Alzheimer's i.e. depending on the form of the gene. Turned out:

• one form of the protein coded by the gene was less susceptible to being cleaved by a protein expressed by gingivitis (lower susceptibility to Alzheimer's). I think this one only had 1 bond which could be cleaved by the gingivitis protein;
• one form of the protein coded by the gene had "normal" susceptibility to being cleaved by a protein expressed by gingivitis (normal susceptibility to Alzheimer's). I think this one had 2 bonds which could be cleaved by the gingivitis protein;
  
• one form of the protein coded by the gene had "increased" susceptibility to being cleaved by a protein expressed by gingivitis (increased susceptibility to Alzheimer's). I think this one had 3 bonds which could be cleaved by the gingivitis protein.

So the GWAS study turned up a gene but it took some time before someone spotted the link to gingivitis/inflammation. Couldn't find that earlier stuff though - most of the papers which appear on a Google search are recent.

 

There is a "syphilis epidemic" in England according to government figures - and numbers do appear to be rising rapidly.

https://www.gov.uk/government/publications/tracking-the-syphilis-epidemic-in-england

In 2010 there were 1617 cases diagnosed which is a rate of 2.9 per 1000.

In 2019 there were 5875 cases diagnosed which is a rate of 10.5 per 1000.

I do remember reading a while ago that some strains of gonorrhea are becoming impossible to treat in the UK because strains of it are spreading that are now immune to all antibiotics. I don't know if this is also true about syphilis.

I think I'm just going to clear my recent search history...

 

Nope, it definitely says per 1000 on the bottom row - I thought it was unusual when I read it. Of course it could be a typo:

 

I realised the numbers were a bit odd but was too lazy to follow up on the idea.

 

Doctors say a lot of BS. It would be nice if a proper trial was made to see if treating these infections slows down disease progression or not. Even in ME we have seen a lot of talk about pathogens for decades but nobody wants to do a proper trial. There is no money for ME, sure, but AD gets billions in funding so that shouldn't be an issue!