Therapeutic potential of neurotrophic factors in Alzheimer’s Disease
Introduction Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia among the elderly population. AD is accompanied with the dysregulation of specific neurotrophic factors (NTFs) and their receptors, which plays a critical role in neuronal deg...
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Published in | Molecular biology reports Vol. 49; no. 3; pp. 2345 - 2357 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Dordrecht
Springer Netherlands
01.03.2022
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | Introduction
Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia among the elderly population. AD is accompanied with the dysregulation of specific neurotrophic factors (NTFs) and their receptors, which plays a critical role in neuronal degeneration. NTFs are small proteins with therapeutic potential for human neurodegenerative diseases. These growth factors are categorized into four families: neurotrophins, neurokines, the glial cell line-derived NTF family of ligands, and the newly discovered cerebral dopamine NTF/mesencephalic astrocyte-derived NTF family. NTFs are capable of preventing cell death in degenerative conditions and can increase the neuronal growth and function in these disorders. Nevertheless, the adverse side effects of NTFs delivery and poor diffusion of these factors in the brain restrict the efficacy of NTFs therapy in clinical situations.
Materials and methods
In this review, we focus on the current advances in the use of NTFs to treat AD and summarize previous experimental and clinical studies for supporting the protective and therapeutic effects of these factors.
Conclusion
Based on reports, NTFs are considered as new and promising candidates for treating AD and AD-associated cognitive impairment. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Review-3 content type line 23 |
ISSN: | 0301-4851 1573-4978 1573-4978 |
DOI: | 10.1007/s11033-021-06968-9 |