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Current and Near-Future Treatment of Alzheimer’s Disease
Recent findings have improved our understanding of the multifactorial nature of AD. While in early asymptomatic stages of AD, increased amyloid-β synthesis and tau hyperphosphorylation play a key role, while in the latter stages of the disease, numerous dysfunctions of homeostatic mechanisms in neur...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Bentham Science Publishers
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9886829/ https://www.ncbi.nlm.nih.gov/pubmed/34856906 http://dx.doi.org/10.2174/1570159X19666211202124239 |
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author | Gąsiorowski, Kazimierz Brokos, Jadwiga Barbara Sochocka, Marta Ochnik, Michał Chojdak-Łukasiewicz, Justyna Zajączkowska, Katarzyna Fułek, Michał Leszek, Jerzy |
author_facet | Gąsiorowski, Kazimierz Brokos, Jadwiga Barbara Sochocka, Marta Ochnik, Michał Chojdak-Łukasiewicz, Justyna Zajączkowska, Katarzyna Fułek, Michał Leszek, Jerzy |
author_sort | Gąsiorowski, Kazimierz |
collection | PubMed |
description | Recent findings have improved our understanding of the multifactorial nature of AD. While in early asymptomatic stages of AD, increased amyloid-β synthesis and tau hyperphosphorylation play a key role, while in the latter stages of the disease, numerous dysfunctions of homeostatic mechanisms in neurons, glial cells, and cerebrovascular endothelium determine the rate of progression of clinical symptoms. The main driving forces of advanced neurodegeneration include increased inflammatory reactions in neurons and glial cells, oxidative stress, deficiencies in neurotrophic growth and regenerative capacity of neurons, brain insulin resistance with disturbed metabolism in neurons, or reduction of the activity of the Wnt-β catenin pathway, which should integrate the homeostatic mechanisms of brain tissue. In order to more effectively inhibit the progress of neurodegeneration, combination therapies consisting of drugs that rectify several above-mentioned dysfunctions should be used. It should be noted that many widely-used drugs from various pharmacological groups, “in addition” to the main therapeutic indications, have a beneficial effect on neurodegeneration and may be introduced into clinical practice in combination therapy of AD. There is hope that complex treatment will effectively inhibit the progression of AD and turn it into a slowly progressing chronic disease. Moreover, as the mechanisms of bidirectional communication between the brain and microbiota are better understood, it is expected that these pathways will be harnessed to provide novel methods to enhance health and treat AD. |
format | Online Article Text |
id | pubmed-9886829 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Bentham Science Publishers |
record_format | MEDLINE/PubMed |
spelling | pubmed-98868292023-02-09 Current and Near-Future Treatment of Alzheimer’s Disease Gąsiorowski, Kazimierz Brokos, Jadwiga Barbara Sochocka, Marta Ochnik, Michał Chojdak-Łukasiewicz, Justyna Zajączkowska, Katarzyna Fułek, Michał Leszek, Jerzy Curr Neuropharmacol Neurology Recent findings have improved our understanding of the multifactorial nature of AD. While in early asymptomatic stages of AD, increased amyloid-β synthesis and tau hyperphosphorylation play a key role, while in the latter stages of the disease, numerous dysfunctions of homeostatic mechanisms in neurons, glial cells, and cerebrovascular endothelium determine the rate of progression of clinical symptoms. The main driving forces of advanced neurodegeneration include increased inflammatory reactions in neurons and glial cells, oxidative stress, deficiencies in neurotrophic growth and regenerative capacity of neurons, brain insulin resistance with disturbed metabolism in neurons, or reduction of the activity of the Wnt-β catenin pathway, which should integrate the homeostatic mechanisms of brain tissue. In order to more effectively inhibit the progress of neurodegeneration, combination therapies consisting of drugs that rectify several above-mentioned dysfunctions should be used. It should be noted that many widely-used drugs from various pharmacological groups, “in addition” to the main therapeutic indications, have a beneficial effect on neurodegeneration and may be introduced into clinical practice in combination therapy of AD. There is hope that complex treatment will effectively inhibit the progression of AD and turn it into a slowly progressing chronic disease. Moreover, as the mechanisms of bidirectional communication between the brain and microbiota are better understood, it is expected that these pathways will be harnessed to provide novel methods to enhance health and treat AD. Bentham Science Publishers 2022-05-16 2022-05-16 /pmc/articles/PMC9886829/ /pubmed/34856906 http://dx.doi.org/10.2174/1570159X19666211202124239 Text en © 2022 Bentham Science Publishers https://creativecommons.org/licenses/by-nc/4.0/ This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited. |
spellingShingle | Neurology Gąsiorowski, Kazimierz Brokos, Jadwiga Barbara Sochocka, Marta Ochnik, Michał Chojdak-Łukasiewicz, Justyna Zajączkowska, Katarzyna Fułek, Michał Leszek, Jerzy Current and Near-Future Treatment of Alzheimer’s Disease |
title | Current and Near-Future Treatment of Alzheimer’s Disease |
title_full | Current and Near-Future Treatment of Alzheimer’s Disease |
title_fullStr | Current and Near-Future Treatment of Alzheimer’s Disease |
title_full_unstemmed | Current and Near-Future Treatment of Alzheimer’s Disease |
title_short | Current and Near-Future Treatment of Alzheimer’s Disease |
title_sort | current and near-future treatment of alzheimer’s disease |
topic | Neurology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9886829/ https://www.ncbi.nlm.nih.gov/pubmed/34856906 http://dx.doi.org/10.2174/1570159X19666211202124239 |
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