Microglia in Alzheimer’s Disease in the Context of Tau Pathology
Microglia are the cells that comprise the innate immune system in the brain. First described more than a century ago, these cells were initially assigned a secondary role in the central nervous system (CNS) with respect to the protagonists, neurons. However, the latest advances have revealed the com...
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| Format: | Article |
| Language: | English |
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MDPI AG
2020-10-01
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| Series: | Biomolecules |
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| Online Access: | https://www.mdpi.com/2218-273X/10/10/1439 |
| _version_ | 1797551088000303104 |
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| author | Juan Ramón Perea Marta Bolós Jesús Avila |
| author_facet | Juan Ramón Perea Marta Bolós Jesús Avila |
| author_sort | Juan Ramón Perea |
| collection | DOAJ |
| description | Microglia are the cells that comprise the innate immune system in the brain. First described more than a century ago, these cells were initially assigned a secondary role in the central nervous system (CNS) with respect to the protagonists, neurons. However, the latest advances have revealed the complexity and importance of microglia in neurodegenerative conditions such as Alzheimer’s disease (AD), the most common form of dementia associated with aging. This pathology is characterized by the accumulation of amyloid-β peptide (Aβ), which forms senile plaques in the neocortex, as well as by the aggregation of hyperphosphorylated tau protein, a process that leads to the development of neurofibrillary tangles (NFTs). Over the past few years, efforts have been focused on studying the interaction between Aβ and microglia, together with the ability of the latter to decrease the levels of this peptide. Given that most clinical trials following this strategy have failed, current endeavors focus on deciphering the molecular mechanisms that trigger the tau-induced inflammatory response of microglia. In this review, we summarize the most recent studies on the physiological and pathological functions of tau protein and microglia. In addition, we analyze the impact of microglial AD-risk genes (<i>APOE</i>, <i>TREM2,</i> and <i>CD33</i>) in tau pathology, and we discuss the role of extracellular soluble tau in neuroinflammation. |
| first_indexed | 2024-03-10T15:39:48Z |
| format | Article |
| id | doaj.art-bb1d2c8d64c244adbc3c0e98c8959011 |
| institution | Directory Open Access Journal |
| issn | 2218-273X |
| language | English |
| last_indexed | 2024-03-10T15:39:48Z |
| publishDate | 2020-10-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Biomolecules |
| spelling | doaj.art-bb1d2c8d64c244adbc3c0e98c89590112023-11-20T16:58:46ZengMDPI AGBiomolecules2218-273X2020-10-011010143910.3390/biom10101439Microglia in Alzheimer’s Disease in the Context of Tau PathologyJuan Ramón Perea0Marta Bolós1Jesús Avila2Department of Molecular Neuropathology, Centro de Biología Molecular “Severo Ochoa” (CSIC-UAM), 1 Nicolás Cabrera, 28049 Madrid, SpainDepartment of Molecular Neuropathology, Centro de Biología Molecular “Severo Ochoa” (CSIC-UAM), 1 Nicolás Cabrera, 28049 Madrid, SpainDepartment of Molecular Neuropathology, Centro de Biología Molecular “Severo Ochoa” (CSIC-UAM), 1 Nicolás Cabrera, 28049 Madrid, SpainMicroglia are the cells that comprise the innate immune system in the brain. First described more than a century ago, these cells were initially assigned a secondary role in the central nervous system (CNS) with respect to the protagonists, neurons. However, the latest advances have revealed the complexity and importance of microglia in neurodegenerative conditions such as Alzheimer’s disease (AD), the most common form of dementia associated with aging. This pathology is characterized by the accumulation of amyloid-β peptide (Aβ), which forms senile plaques in the neocortex, as well as by the aggregation of hyperphosphorylated tau protein, a process that leads to the development of neurofibrillary tangles (NFTs). Over the past few years, efforts have been focused on studying the interaction between Aβ and microglia, together with the ability of the latter to decrease the levels of this peptide. Given that most clinical trials following this strategy have failed, current endeavors focus on deciphering the molecular mechanisms that trigger the tau-induced inflammatory response of microglia. In this review, we summarize the most recent studies on the physiological and pathological functions of tau protein and microglia. In addition, we analyze the impact of microglial AD-risk genes (<i>APOE</i>, <i>TREM2,</i> and <i>CD33</i>) in tau pathology, and we discuss the role of extracellular soluble tau in neuroinflammation.https://www.mdpi.com/2218-273X/10/10/1439Alzheimer’s diseasetauopathiestauAβmicroglianeuroinflammation |
| spellingShingle | Juan Ramón Perea Marta Bolós Jesús Avila Microglia in Alzheimer’s Disease in the Context of Tau Pathology Biomolecules Alzheimer’s disease tauopathies tau Aβ microglia neuroinflammation |
| title | Microglia in Alzheimer’s Disease in the Context of Tau Pathology |
| title_full | Microglia in Alzheimer’s Disease in the Context of Tau Pathology |
| title_fullStr | Microglia in Alzheimer’s Disease in the Context of Tau Pathology |
| title_full_unstemmed | Microglia in Alzheimer’s Disease in the Context of Tau Pathology |
| title_short | Microglia in Alzheimer’s Disease in the Context of Tau Pathology |
| title_sort | microglia in alzheimer s disease in the context of tau pathology |
| topic | Alzheimer’s disease tauopathies tau Aβ microglia neuroinflammation |
| url | https://www.mdpi.com/2218-273X/10/10/1439 |
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