Mechanisms Involved in Microglial-Interceded Alzheimer’s Disease and Nanocarrier-Based Treatment Approaches Article Swipe
Shadab Md
,
Nabil A. Alhakamy
,
Mohamed A. Alfaleh
,
Obaid Afzal
,
Abdulmalik Saleh Alfawaz Altamimi
,
Ashif Iqubal
,
Rasheed A. Shaik
·
YOU?
·
· 2021
· Open Access
·
· DOI: https://doi.org/10.3390/jpm11111116
YOU?
·
· 2021
· Open Access
·
· DOI: https://doi.org/10.3390/jpm11111116
Alzheimer’s disease (AD) is a common neurodegenerative disorder accountable for dementia and cognitive dysfunction. The etiology of AD is complex and multifactorial in origin. The formation and deposition of amyloid-beta (Aβ), hyperphosphorylated tau protein, neuroinflammation, persistent oxidative stress, and alteration in signaling pathways have been extensively explored among the various etiological hallmarks. However, more recently, the immunogenic regulation of AD has been identified, and macroglial activation is considered a limiting factor in its etiological cascade. Macroglial activation causes neuroinflammation via modulation of the NLRP3/NF-kB/p38 MAPKs pathway and is also involved in tau pathology via modulation of the GSK-3β/p38 MAPK pathways. Additionally, microglial activation contributes to the discrete release of neurotransmitters and an altered neuronal synaptic plasticity. Therefore, activated microglial cells appear to be an emerging target for managing and treating AD. This review article discussed the pathology of microglial activation in AD and the role of various nanocarrier-based anti-Alzeihmenr’s therapeutic approaches that can either reverse or inhibit this activation. Thus, as a targeted drug delivery system, nanocarrier approaches could emerge as a novel means to overcome existing AD therapy limitations.
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Metadata
- Type
- review
- Language
- en
- Landing Page
- https://doi.org/10.3390/jpm11111116
- https://www.mdpi.com/2075-4426/11/11/1116/pdf?version=1635848675
- OA Status
- gold
- Cited By
- 21
- References
- 244
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W3211092327
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Raw OpenAlex JSON
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https://openalex.org/W3211092327Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.3390/jpm11111116Digital Object Identifier
- Title
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Mechanisms Involved in Microglial-Interceded Alzheimer’s Disease and Nanocarrier-Based Treatment ApproachesWork title
- Type
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reviewOpenAlex work type
- Language
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enPrimary language
- Publication year
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2021Year of publication
- Publication date
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2021-10-29Full publication date if available
- Authors
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Shadab Md, Nabil A. Alhakamy, Mohamed A. Alfaleh, Obaid Afzal, Abdulmalik Saleh Alfawaz Altamimi, Ashif Iqubal, Rasheed A. ShaikList of authors in order
- Landing page
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https://doi.org/10.3390/jpm11111116Publisher landing page
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https://www.mdpi.com/2075-4426/11/11/1116/pdf?version=1635848675Direct link to full text PDF
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YesWhether a free full text is available
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goldOpen access status per OpenAlex
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https://www.mdpi.com/2075-4426/11/11/1116/pdf?version=1635848675Direct OA link when available
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Neuroinflammation, Neuroscience, Nanocarriers, Dementia, Synaptic plasticity, Medicine, Signal transduction, Neurodegeneration, Disease, Biology, Cell biology, Pharmacology, Pathology, Drug, Receptor, Internal medicineTop concepts (fields/topics) attached by OpenAlex
- Cited by
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21Total citation count in OpenAlex
- Citations by year (recent)
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2025: 11, 2024: 2, 2023: 3, 2022: 5Per-year citation counts (last 5 years)
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244Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.alteration | 39 |
| abstract_inverted_index.approaches | 150, 167 |
| abstract_inverted_index.considered | 67 |
| abstract_inverted_index.deposition | 27 |
| abstract_inverted_index.hallmarks. | 51 |
| abstract_inverted_index.macroglial | 64 |
| abstract_inverted_index.microglial | 101, 118, 138 |
| abstract_inverted_index.modulation | 80, 94 |
| abstract_inverted_index.persistent | 35 |
| abstract_inverted_index.regulation | 57 |
| abstract_inverted_index.GSK-3β/p38 | 97 |
| abstract_inverted_index.accountable | 8 |
| abstract_inverted_index.activation. | 158 |
| abstract_inverted_index.contributes | 103 |
| abstract_inverted_index.etiological | 50, 73 |
| abstract_inverted_index.extensively | 45 |
| abstract_inverted_index.identified, | 62 |
| abstract_inverted_index.immunogenic | 56 |
| abstract_inverted_index.nanocarrier | 166 |
| abstract_inverted_index.plasticity. | 115 |
| abstract_inverted_index.therapeutic | 149 |
| abstract_inverted_index.amyloid-beta | 29 |
| abstract_inverted_index.dysfunction. | 13 |
| abstract_inverted_index.limitations. | 179 |
| abstract_inverted_index.Additionally, | 100 |
| abstract_inverted_index.Alzheimer’s | 0 |
| abstract_inverted_index.multifactorial | 21 |
| abstract_inverted_index.NLRP3/NF-kB/p38 | 83 |
| abstract_inverted_index.nanocarrier-based | 147 |
| abstract_inverted_index.neurodegenerative | 6 |
| abstract_inverted_index.neuroinflammation | 78 |
| abstract_inverted_index.neurotransmitters | 109 |
| abstract_inverted_index.neuroinflammation, | 34 |
| abstract_inverted_index.anti-Alzeihmenr’s | 148 |
| abstract_inverted_index.hyperphosphorylated | 31 |
| cited_by_percentile_year.max | 99 |
| cited_by_percentile_year.min | 94 |
| corresponding_author_ids | https://openalex.org/A5023348528 |
| countries_distinct_count | 2 |
| institutions_distinct_count | 7 |
| corresponding_institution_ids | https://openalex.org/I185163786 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.8399999737739563 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.7451013 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |