Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, August 2, 2025

Biofilm-associated proteins: from the gut biofilms to neurodegeneration

 17 pages at the link which your competent? doctor will distill into EXACT PREVENTION PROTOCOLS, right? Oh no, NOTHING HAPPENED, LIKE USUAL!

Do you prefer your doctor and hospital incompetence NOT KNOWING? OR NOT DOING?

The reason you need dementia prevention: 

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.

3. A 20% chance in this research.   July 2013. 

Biofilm-associated proteins: from the gut biofilms to neurodegeneration

AuthorsValle Turrillas, Jaione CSIC ORCID 
FundersAgencia Estatal de Investigación (España)
Ministerio de Ciencia e Innovación (España)
KeywordsAmyloid
Biofilm
Biofilm-associated protein
Gut microbiota
α-synuclein
Issue DateDec-2025
PublisherTaylor & Francis
CitationGut Microbes 17(1): 2461721 (2025)
AbstractHuman microbiota form a biofilm with substantial consequences for health and disease. Numerous studies have indicated that microbial communities produce functional amyloids as part of their biofilm extracellular scaffolds. The overlooked interplay between bacterial amyloids and the host may have detrimental consequences for the host, including neurodegeneration. This work gives an overview of the biofilm-associated amyloids expressed by the gut microbiota and their potential role in neurodegeneration. It discusses the biofilm-associated proteins (BAPs) of the gut microbiota, maps the amyloidogenic domains of these proteins, and analyzes the presence of bap genes within accessory genomes linked with transposable elements. Furthermore, the evidence supporting the existence of amyloids in the gut are presented. Finally, it explores the potential interactions between BAPs and α-synuclein, extending the literature on amyloid cross-kingdom interactions. Based on these findings, this study propose that BAP amyloids act as transmissible catalysts, facilitating the misfolding, accumulation, and spread of α-synuclein aggregates. This review contributes to the understanding of complex interactions among the microbiota, transmissible elements, and host, which is crucial for developing novel therapeutic approaches to combat microbiota-related diseases and improve overall health outcomes.
Publisher version (URL)https://doi.org/10.1080/19490976.2025.2461721
URIhttp://hdl.handle.net/10261/396268
DOI10.1080/19490976.2025.2461721
ISSN1949-0976
E-ISSN1949-0984
User licensehttps://creativecommons.org/licenses/by/4.0/
Source worksThe underlying dataset has been published as supplementary material of the article in the publisher platform at https://doi.org/10.1080/19490976.2025.2461721© 2025 CSIC. Published with license by Taylor & Francis Group, LLC.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the AcceptedManuscript in a repository by the author(s) or with their consent.
Appears in Collections:(IDAB) Artículos

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