Dissecting the Crosstalk between Endothelial Mitochondrial Damage, Vascular Inflammation, and Neurodegeneration in Cerebral Amyloid Angiopathy and Alzheimer’s Disease

Alzheimer’s disease (AD) is the most prevalent cause of dementia and is pathologically characterized by the presence of parenchymal senile plaques composed of amyloid β (Aβ) and intraneuronal neurofibrillary tangles of hyperphosphorylated tau protein. The accumulation of Aβ also occurs within the ce...

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Autores principales:	Rebecca M. Parodi-Rullán, Sabzali Javadov, Silvia Fossati
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	mitochondria Alzheimer’s disease cerebral amyloid angiopathy inflammation neurodegeneration amyloid Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/5a0aa6ebc9904801a7708717e98fd92a
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spelling	oai:doaj.org-article:5a0aa6ebc9904801a7708717e98fd92a2021-11-25T17:08:43ZDissecting the Crosstalk between Endothelial Mitochondrial Damage, Vascular Inflammation, and Neurodegeneration in Cerebral Amyloid Angiopathy and Alzheimer’s Disease10.3390/cells101129032073-4409https://doaj.org/article/5a0aa6ebc9904801a7708717e98fd92a2021-10-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/2903https://doaj.org/toc/2073-4409Alzheimer’s disease (AD) is the most prevalent cause of dementia and is pathologically characterized by the presence of parenchymal senile plaques composed of amyloid β (Aβ) and intraneuronal neurofibrillary tangles of hyperphosphorylated tau protein. The accumulation of Aβ also occurs within the cerebral vasculature in over 80% of AD patients and in non-demented individuals, a condition called cerebral amyloid angiopathy (CAA). The development of CAA is associated with neurovascular dysfunction, blood–brain barrier (BBB) leakage, and persistent vascular- and neuro-inflammation, eventually leading to neurodegeneration. Although pathologically AD and CAA are well characterized diseases, the chronology of molecular changes that lead to their development is still unclear. Substantial evidence demonstrates defects in mitochondrial function in various cells of the neurovascular unit as well as in the brain parenchyma during the early stages of AD and CAA. Dysfunctional mitochondria release danger-associated molecular patterns (DAMPs) that activate a wide range of inflammatory pathways. In this review, we gather evidence to postulate a crucial role of the mitochondria, specifically of cerebral endothelial cells, as sensors and initiators of Aβ-induced vascular inflammation. The activated vasculature recruits circulating immune cells into the brain parenchyma, leading to the development of neuroinflammation and neurodegeneration in AD and CAA.Rebecca M. Parodi-RullánSabzali JavadovSilvia FossatiMDPI AGarticlemitochondriaAlzheimer’s diseasecerebral amyloid angiopathyinflammationneurodegenerationamyloidBiology (General)QH301-705.5ENCells, Vol 10, Iss 2903, p 2903 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	mitochondria Alzheimer’s disease cerebral amyloid angiopathy inflammation neurodegeneration amyloid Biology (General) QH301-705.5
spellingShingle	mitochondria Alzheimer’s disease cerebral amyloid angiopathy inflammation neurodegeneration amyloid Biology (General) QH301-705.5 Rebecca M. Parodi-Rullán Sabzali Javadov Silvia Fossati Dissecting the Crosstalk between Endothelial Mitochondrial Damage, Vascular Inflammation, and Neurodegeneration in Cerebral Amyloid Angiopathy and Alzheimer’s Disease
description	Alzheimer’s disease (AD) is the most prevalent cause of dementia and is pathologically characterized by the presence of parenchymal senile plaques composed of amyloid β (Aβ) and intraneuronal neurofibrillary tangles of hyperphosphorylated tau protein. The accumulation of Aβ also occurs within the cerebral vasculature in over 80% of AD patients and in non-demented individuals, a condition called cerebral amyloid angiopathy (CAA). The development of CAA is associated with neurovascular dysfunction, blood–brain barrier (BBB) leakage, and persistent vascular- and neuro-inflammation, eventually leading to neurodegeneration. Although pathologically AD and CAA are well characterized diseases, the chronology of molecular changes that lead to their development is still unclear. Substantial evidence demonstrates defects in mitochondrial function in various cells of the neurovascular unit as well as in the brain parenchyma during the early stages of AD and CAA. Dysfunctional mitochondria release danger-associated molecular patterns (DAMPs) that activate a wide range of inflammatory pathways. In this review, we gather evidence to postulate a crucial role of the mitochondria, specifically of cerebral endothelial cells, as sensors and initiators of Aβ-induced vascular inflammation. The activated vasculature recruits circulating immune cells into the brain parenchyma, leading to the development of neuroinflammation and neurodegeneration in AD and CAA.
format	article
author	Rebecca M. Parodi-Rullán Sabzali Javadov Silvia Fossati
author_facet	Rebecca M. Parodi-Rullán Sabzali Javadov Silvia Fossati
author_sort	Rebecca M. Parodi-Rullán
title	Dissecting the Crosstalk between Endothelial Mitochondrial Damage, Vascular Inflammation, and Neurodegeneration in Cerebral Amyloid Angiopathy and Alzheimer’s Disease
title_short	Dissecting the Crosstalk between Endothelial Mitochondrial Damage, Vascular Inflammation, and Neurodegeneration in Cerebral Amyloid Angiopathy and Alzheimer’s Disease
title_full	Dissecting the Crosstalk between Endothelial Mitochondrial Damage, Vascular Inflammation, and Neurodegeneration in Cerebral Amyloid Angiopathy and Alzheimer’s Disease
title_fullStr	Dissecting the Crosstalk between Endothelial Mitochondrial Damage, Vascular Inflammation, and Neurodegeneration in Cerebral Amyloid Angiopathy and Alzheimer’s Disease
title_full_unstemmed	Dissecting the Crosstalk between Endothelial Mitochondrial Damage, Vascular Inflammation, and Neurodegeneration in Cerebral Amyloid Angiopathy and Alzheimer’s Disease
title_sort	dissecting the crosstalk between endothelial mitochondrial damage, vascular inflammation, and neurodegeneration in cerebral amyloid angiopathy and alzheimer’s disease
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/5a0aa6ebc9904801a7708717e98fd92a
work_keys_str_mv	AT rebeccamparodirullan dissectingthecrosstalkbetweenendothelialmitochondrialdamagevascularinflammationandneurodegenerationincerebralamyloidangiopathyandalzheimersdisease AT sabzalijavadov dissectingthecrosstalkbetweenendothelialmitochondrialdamagevascularinflammationandneurodegenerationincerebralamyloidangiopathyandalzheimersdisease AT silviafossati dissectingthecrosstalkbetweenendothelialmitochondrialdamagevascularinflammationandneurodegenerationincerebralamyloidangiopathyandalzheimersdisease
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Dissecting the Crosstalk between Endothelial Mitochondrial Damage, Vascular Inflammation, and Neurodegeneration in Cerebral Amyloid Angiopathy and Alzheimer’s Disease

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