The neurovascular unit dysfunction in Alzheimer’s disease

Luis O. Soto-Rojas, Mar Pacheco-Herrero, Paola A. Martínez-Gómez, B. Berenice Campa-Córdoba, Ricardo Apátiga-Pérez, Marcos M. Villegas-Rojas, Charles R. Harrington, Fidel de la Cruz, Linda Garcés-Ramírez, José Luna-Muñoz

Research output: Contribution to journalReview articlepeer-review

2 Scopus citations


Alzheimer’s disease (AD) is the most common neurodegenerative disease worldwide. Histopathologically, AD presents with two hallmarks: neurofibrillary tangles (NFTs), and aggregates of amyloid β peptide (Aβ) both in the brain parenchyma as neuritic plaques, and around blood vessels as cerebral amyloid angiopathy (CAA). According to the vascular hypothesis of AD, vascular risk factors can result in dysregulation of the neurovascular unit (NVU) and hypoxia. Hypoxia may reduce Aβ clearance from the brain and increase its production, leading to both parenchymal and vascular accumulation of Aβ. An increase in Aβ amplifies neuronal dysfunction, NFT for-mation, and accelerates neurodegeneration, resulting in dementia. In recent decades, therapeutic approaches have attempted to decrease the levels of abnormal Aβ or tau levels in the AD brain. However, several of these approaches have either been associated with an inappropriate immune response triggering inflammation, or have failed to improve cognition. Here, we review the patho-genesis and potential therapeutic targets associated with dysfunction of the NVU in AD.

Original languageEnglish
Article number2022
Pages (from-to)1-27
Number of pages27
JournalInternational Journal of Molecular Sciences
Issue number4
StatePublished - 2 Feb 2021


  • Alzheimer’s disease
  • Amyloid peptide
  • Astrocytes
  • Blood-brain barrier
  • Microglia
  • Tau protein


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