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Technical report
peer-reviewed

Mechanical Dilution of Beta-amyloid Peptide and Phosphorylated Tau Protein in Alzheimer's Disease: Too Simple to be True?



Abstract

The neuropathology of Alzheimer's disease (AD) is characterized by the widespread accumulation of neuritic plaques and neurofibrillary tangles composed of deposits of beta-amyloid peptide (Aβ) and abnormally phosphorylated tau protein (phospho-tau) respectively. Considerable effort has been expended to identify methods to retard the deposition of these proteins or to enhance their clearance. It is strikingly surprising that until now, very few researchers have attempted to remove these proteins using mechanical procedures.

In this article, we start by showing the rationale of mechanical dilution of cerebrospinal fluid (CSF) as a therapeutic approach in AD. Then, we present models of implantable systems allowing mechanical dilution of CSF by means of CSF replacement and CSF filtration (liquorpheresis). We conclude that even though this approach seems simplistic, it is feasible and deserves exploration.



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Technical report
peer-reviewed

Mechanical Dilution of Beta-amyloid Peptide and Phosphorylated Tau Protein in Alzheimer's Disease: Too Simple to be True?


Author Information

Manuel Menéndez González Corresponding Author

Neurology, Hospital Universitario Central de Asturias

Morphology and Cellular Biology, Universidad de Oviedo

Facultad de Ciencias de la Salud, Universidad Autónoma de Chile


Ethics Statement and Conflict of Interest Disclosures

Human subjects: This study did not involve human participants or tissue. Animal subjects: This study did not involve animal subjects or tissue. Conflicts of interest: The authors have declared that no conflicts of interest exist.


Technical report
peer-reviewed

Mechanical Dilution of Beta-amyloid Peptide and Phosphorylated Tau Protein in Alzheimer's Disease: Too Simple to be True?


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Technical report
peer-reviewed

Mechanical Dilution of Beta-amyloid Peptide and Phosphorylated Tau Protein in Alzheimer's Disease: Too Simple to be True?

  • Author Information
    Manuel Menéndez González Corresponding Author

    Neurology, Hospital Universitario Central de Asturias

    Morphology and Cellular Biology, Universidad de Oviedo

    Facultad de Ciencias de la Salud, Universidad Autónoma de Chile


    Ethics Statement and Conflict of Interest Disclosures

    Human subjects: This study did not involve human participants or tissue. Animal subjects: This study did not involve animal subjects or tissue. Conflicts of interest: The authors have declared that no conflicts of interest exist.

    Acknowledgements


    Article Information

    Published: February 28, 2017

    DOI

    10.7759/cureus.1062

    Cite this article as:

    Menéndez gonzález M (February 28, 2017) Mechanical Dilution of Beta-amyloid Peptide and Phosphorylated Tau Protein in Alzheimer's Disease: Too Simple to be True?. Cureus 9(2): e1062. doi:10.7759/cureus.1062

    Publication history

    Received by Cureus: December 22, 2016
    Peer review began: January 04, 2017
    Peer review concluded: February 19, 2017
    Published: February 28, 2017

    Copyright

    © Copyright 2017
    Menéndez González. This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 3.0., which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

    License

    This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The neuropathology of Alzheimer's disease (AD) is characterized by the widespread accumulation of neuritic plaques and neurofibrillary tangles composed of deposits of beta-amyloid peptide (Aβ) and abnormally phosphorylated tau protein (phospho-tau) respectively. Considerable effort has been expended to identify methods to retard the deposition of these proteins or to enhance their clearance. It is strikingly surprising that until now, very few researchers have attempted to remove these proteins using mechanical procedures.

In this article, we start by showing the rationale of mechanical dilution of cerebrospinal fluid (CSF) as a therapeutic approach in AD. Then, we present models of implantable systems allowing mechanical dilution of CSF by means of CSF replacement and CSF filtration (liquorpheresis). We conclude that even though this approach seems simplistic, it is feasible and deserves exploration.



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Create a free account to continue reading this article.

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Manuel Menéndez González

Neurology, Hospital Universitario Central de Asturias

For correspondence:
manuelmenendezgonzalez@gmail.com

Manuel Menéndez González

Neurology, Hospital Universitario Central de Asturias

For correspondence:
manuelmenendezgonzalez@gmail.com