Alzheimer and brain infection

Insights and discussion from the cutting edge with reference to journal articles and other research papers.
circular
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Re: Alzheimer and brain infection

Post by circular »

rws wrote:
circular wrote:This is ever so interesting. Now that I understand (at least I think I read this in the last several days) that there's no blood-brain barrier via the nose...
It's not exactly the nose, see
https://en.wikipedia.org/wiki/Danger_tr ... f_the_face
Thanks, interesting explanation.
Due to the special nature of the blood supply to the human nose and surrounding area, it is possible, albeit extremely unlikely, for retrograde infections from the nasal area to spread to the brain, causing cavernous sinus thrombosis, meningitis or brain abscess.
This writer seems to be just looking for rather severe infections and I wonder if s/he's missing the possibility of more chronic, low-grade ones via this the avenue described.

(I later saw that it was in this thread where I'd read about no BBB in this area.)
ApoE 3/4 > Thanks in advance for any responses made to my posts.
rws
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Re: Alzheimer and brain infection

Post by rws »

circular wrote:
Due to the special nature of the blood supply to the human nose and surrounding area, it is possible, albeit extremely unlikely, for retrograde infections from the nasal area to spread to the brain, causing cavernous sinus thrombosis, meningitis or brain abscess.
This writer seems to be just looking for rather severe infections and I wonder if s/he's missing the possibility of more chronic, low-grade ones via this the avenue described.
That was my thought as well. The first candidate obviously would be Propionibacterium acnes. But how to test this hypothesis? Ask people if they tend to pop their pimples? And what if there is an association with AD? Can you imagine the headlines?
circular
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Re: Alzheimer and brain infection

Post by circular »

Back when I read about that acne bacteria I also almost posted 'Can you imagine the headlines about acne causing Alzheimer's'? Happy to share wavelengths with you ;)
ApoE 3/4 > Thanks in advance for any responses made to my posts.
rws
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Re: Alzheimer and brain infection

Post by rws »

For completeness of this thread here are two papers by Miklossy.

Miklossy J. Bacterial amyloid and DNA are important constituents of senile plaques: further evidence of the spirochetal and biofilm nature of senile plaques. J Alzheimers Dis. 2016; 53:1459–1473.
http://content.iospress.com/articles/jo ... /jad160451

"... Aβ and DNA, including spirochete-specific DNA, are key components of both pure spirochetal biofilms and senile plaques in AD and confirm the biofilm nature of senile plaques."
I have the impression the author is a bit too focused on amyloid. If I were him I would be more interested in how and when Borrelia burgdorferi gets where he found it.

Miklossy J. Historic evidence to support a causal relationship between spirochetal infections and Alzheimer’s disease. Front Aging Neurosci. 2015; 7:46.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4399390/

"Historic observations and illustrations published in the first half of the 20th Century indeed confirm that the pathological hallmarks, which define AD, are also present in syphilitic dementia."
rws
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Re: Alzheimer and brain infection

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During sepsis the blood-brain-barrier is permeable but the bacteria they found did not stay there in surviving mice. So the innate immune response in the brain works. They did not test for fungi however.

Bacterial Dissemination to the Brain in Sepsis
Benjamin H Singer , Robert P. Dickson , Scott J Denstaedt , Michael W. Newstead , Kwi Kim , Nicole R Falkowski , John R Erb-Downward , Thomas M Schmidt , Gary B. Huffnagle , and Theodore J. Standiford
https://www.ncbi.nlm.nih.gov/pubmed/29232157
http://www.atsjournals.org/doi/abs/10.1 ... 708-1559OC
rws
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Re: Alzheimer and brain infection

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The Physiological Roles of Amyloid-β Peptide Hint at New Ways to Treat Alzheimer's Disease
Brothers Holly M., Gosztyla Maya L., Robinson Stephen R.
Frontiers in Aging Neuroscience 10(2018), 118
https://www.frontiersin.org/article/10. ... 2018.00118
DOI=10.3389/fnagi.2018.00118

ABSTRACT=Amyloid-ß (Aß) is best known as the misfolded peptide that is involved in the pathogenesis of Alzheimer's disease (AD), and it is currently the primary therapeutic target in attempts to arrest the course of this disease. This notoriety has overshadowed evidence that Aß serves several important physiological functions. Aß is present throughout the lifespan, it has been found in all vertebrates examined thus far, and its molecular sequence shows a high degree of conservation. These features are typical of a factor that contributes significantly to biological fitness, and this suggestion has been supported by evidence of functions that are beneficial for the brain. The putative roles of Aß include protecting the body from infections, repairing leaks in the blood-brain barrier, promoting recovery from injury, and regulating synaptic function. Evidence for these beneficial roles comes from in vitro and in vivo studies, which have shown that the cellular production of Aß rapidly increases in response to a physiological challenge and often diminishes upon recovery. These roles are further supported by the adverse outcomes of clinical trials that have attempted to deplete Aß in order to treat AD. We suggest that anti-Aß therapies will produce fewer adverse effects if the known triggers of Aß deposition (e.g. pathogens, hypertension and diabetes) are addressed first.
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