Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2022:273:247-266.
doi: 10.1007/164_2020_418.

The Blood-Brain Barrier in Alzheimer's Disease

Affiliations

The Blood-Brain Barrier in Alzheimer's Disease

Steffen E Storck et al. Handb Exp Pharmacol. 2022.

Abstract

The accumulation of neurotoxic amyloid-beta (Aβ) in the brain is one of the characteristic hallmarks of Alzheimer's disease (AD). Aβ-peptide brain homeostasis is governed by its production and various clearance mechanisms. The blood-brain barrier provides a large surface area for influx and efflux mechanisms into and out of the brain. Different transporters and receptors have been implicated to play crucial roles in Aβ clearance from brain. Besides Aβ transport, the blood-brain barrier tightly regulates the brain's microenvironment; however, vascular alterations have been shown in patients with AD. Here, we summarize how the blood-brain barrier changes during aging and in disease and focus on recent findings of how the ABC transporter P-glycoprotein (ABCB1/P-gp) and the receptor low-density lipoprotein receptor-related protein 1 (LRP1) play a role in Aβ clearance from brain.

Keywords: Alzheimer’s disease (AD); Amyloid-beta (Aβ); Blood-brain barrier; Clearance; LRP1; Neurovascular unit; P-gp/ABCB1.

PubMed Disclaimer

References

    1. Abbott NJ, Pizzo ME, Preston JE, Janigro D, Thorne RG (2018) The role of brain barriers in fluid movement in the CNS: is there a ‘glymphatic’ system? Acta Neuropathol 135(3):387–407. 10.1007/s00401-018-1812-4 - DOI - PubMed
    1. Alzheimer A (1906) Über einen eigenartigen schweren Erkrankungsprozeß der Hirnrind. Neurologisches Centralblatt 23:1129–1136
    1. Alzheimer A (1907) Über eine eigenartige Erkrankung der Hirnrinde. Allgemeine Zeitschrift für Psychiatrie und Psychisch-Gerichtliche Medizin 64:146–148
    1. Barakat S, Demeule M, Pilorget A, Regina A, Gingras D, Baggetto LG, Beliveau R (2007) Modulation of p-glycoprotein function by caveolin-1 phosphorylation. J Neurochem 101 (1):1–8. 10.1111/j.1471-4159.2006.04410.x - DOI - PubMed
    1. Barthelemy NR, Li Y, Joseph-Mathurin N, Gordon BA, Hassenstab J, Benzinger TLS, Dominantly Inherited Alzheimer, N (2020) A soluble phosphorylated tau signature links tau, amyloid and the evolution of stages of dominantly inherited Alzheimer’s disease. [Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov’t]. Nat Med 26(3):398–407. 10.1038/s41591-020-0781-z - DOI - PMC - PubMed