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      Evolution of blood–brain barrier in brain diseases and related systemic nanoscale brain-targeting drug delivery strategies

      review-article
      Author(s): a , ∗ , b
      Publication date (Electronic):
      Journal: Acta Pharmaceutica Sinica. B
      Publisher: Elsevier
      Keywords: Blood–brain barrier, Brain diseases, Brain-targeting, Drug delivery systems, Nanoparticles, Aβ, amyloid beta, AD, Alzheimer's disease, AMT, alpha-methyl-l-tryptophan, BACE1, β-secretase 1, BBB, blood–brain barrier, BDNF, brain derived neurotrophic factor, BTB, blood–brain tumor barrier, CMT, carrier-mediated transportation, DTPA-Gd, Gd-diethyltriaminepentaacetic acid, EPR, enhanced permeability and retention, Gd, gadolinium, GLUT1, glucose transporter-1, ICAM-1, intercellular adhesion molecule-1, KATP, ATP-sensitive potassium channels, KCa, calcium-dependent potassium channels, LAT1, L-type amino acid transporter 1, LDL, low density lipoprotein, LDLR, LDL receptor, LFA-1, lymphocyte function associated antigen-1, LRP1, LDLR-related protein 1, MFSD2A, major facilitator superfamily domain-containing protein 2a, MMP9, metalloproteinase-9, MRI, magnetic resonance imaging, NPs, nanoparticles, PD, Parkinson's disease, PEG, polyethyleneglycol, PEG-PLGA, polyethyleneglycol-poly(lactic-co-glycolic acid), P-gp, P-glycoprotein, PLGA, poly(lactic-co-glycolic acid), PSMA, prostate-specific membrane antigen, RAGE, receptor for advanced glycosylation end products, RBC, red blood cell, RMT, receptor-mediated transcytosis, ROS, reactive oxygen species, siRNA, short interfering RNA, TBI, traumatic brain injury, TfR, transferrin receptor, TJ, tight junction, tPA, tissue plasminogen activator, VEGF, vascular endothelial growth factor, ZO1, zona occludens 1

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          Abstract

          Blood–brain barrier (BBB) strictly controls matter exchange between blood and brain, and severely limits brain penetration of systemically administered drugs, resulting in ineffective drug therapy of brain diseases. However, during the onset and progression of brain diseases, BBB alterations evolve inevitably. In this review, we focus on nanoscale brain-targeting drug delivery strategies designed based on BBB evolutions and related applications in various brain diseases including Alzheimer's disease, Parkinson's disease, epilepsy, stroke, traumatic brain injury and brain tumor. The advances on optimization of small molecules for BBB crossing and non-systemic administration routes ( e. g., intranasal treatment) for BBB bypassing are not included in this review.

          Graphical abstract

          Blood–brain barrier (BBB) is evolving during the onset and progression of brain diseases. BBB evolution-based nanoscale brain-targeting drug delivery strategies are summarized in this review for various brain diseases.

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          Blood–brain barrier breakdown in Alzheimer disease and other neurodegenerative disorders

          Melanie D Sweeney, Berislav Zlokovic, Abhay Sagare (2018)
          The blood-brain barrier (BBB) is a continuous endothelial membrane within brain microvessels that has sealed cell-to-cell contacts and is sheathed by mural vascular cells and perivascular astrocyte end-feet. The BBB protects neurons from factors present in the systemic circulation and maintains the highly regulated CNS internal milieu, which is required for proper synaptic and neuronal functioning. BBB disruption allows influx into the brain of neurotoxic blood-derived debris, cells and microbial pathogens and is associated with inflammatory and immune responses, which can initiate multiple pathways of neurodegeneration. This Review discusses neuroimaging studies in the living human brain and post-mortem tissue as well as biomarker studies demonstrating BBB breakdown in Alzheimer disease, Parkinson disease, Huntington disease, amyotrophic lateral sclerosis, multiple sclerosis, HIV-1-associated dementia and chronic traumatic encephalopathy. The pathogenic mechanisms by which BBB breakdown leads to neuronal injury, synaptic dysfunction, loss of neuronal connectivity and neurodegeneration are described. The importance of a healthy BBB for therapeutic drug delivery and the adverse effects of disease-initiated, pathological BBB breakdown in relation to brain delivery of neuropharmaceuticals are briefly discussed. Finally, future directions, gaps in the field and opportunities to control the course of neurological diseases by targeting the BBB are presented.
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            Structure and function of the blood-brain barrier.

            N. Abbott, Adjanie Patabendige, Diana Dolman … (2010)
            Neural signalling within the central nervous system (CNS) requires a highly controlled microenvironment. Cells at three key interfaces form barriers between the blood and the CNS: the blood-brain barrier (BBB), blood-CSF barrier and the arachnoid barrier. The BBB at the level of brain microvessel endothelium is the major site of blood-CNS exchange. The structure and function of the BBB is summarised, the physical barrier formed by the endothelial tight junctions, and the transport barrier resulting from membrane transporters and vesicular mechanisms. The roles of associated cells are outlined, especially the endfeet of astrocytic glial cells, and pericytes and microglia. The embryonic development of the BBB, and changes in pathology are described. The BBB is subject to short and long-term regulation, which may be disturbed in pathology. Any programme for drug discovery or delivery, to target or avoid the CNS, needs to consider the special features of the BBB.
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              Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke.

              Werner Hacke, Markku Kaste, Erich Bluhmki … (2008)
              Intravenous thrombolysis with alteplase is the only approved treatment for acute ischemic stroke, but its efficacy and safety when administered more than 3 hours after the onset of symptoms have not been established. We tested the efficacy and safety of alteplase administered between 3 and 4.5 hours after the onset of a stroke. After exclusion of patients with a brain hemorrhage or major infarction, as detected on a computed tomographic scan, we randomly assigned patients with acute ischemic stroke in a 1:1 double-blind fashion to receive treatment with intravenous alteplase (0.9 mg per kilogram of body weight) or placebo. The primary end point was disability at 90 days, dichotomized as a favorable outcome (a score of 0 or 1 on the modified Rankin scale, which has a range of 0 to 6, with 0 indicating no symptoms at all and 6 indicating death) or an unfavorable outcome (a score of 2 to 6 on the modified Rankin scale). The secondary end point was a global outcome analysis of four neurologic and disability scores combined. Safety end points included death, symptomatic intracranial hemorrhage, and other serious adverse events. We enrolled a total of 821 patients in the study and randomly assigned 418 to the alteplase group and 403 to the placebo group. The median time for the administration of alteplase was 3 hours 59 minutes. More patients had a favorable outcome with alteplase than with placebo (52.4% vs. 45.2%; odds ratio, 1.34; 95% confidence interval [CI], 1.02 to 1.76; P=0.04). In the global analysis, the outcome was also improved with alteplase as compared with placebo (odds ratio, 1.28; 95% CI, 1.00 to 1.65; P<0.05). The incidence of intracranial hemorrhage was higher with alteplase than with placebo (for any intracranial hemorrhage, 27.0% vs. 17.6%; P=0.001; for symptomatic intracranial hemorrhage, 2.4% vs. 0.2%; P=0.008). Mortality did not differ significantly between the alteplase and placebo groups (7.7% and 8.4%, respectively; P=0.68). There was no significant difference in the rate of other serious adverse events. As compared with placebo, intravenous alteplase administered between 3 and 4.5 hours after the onset of symptoms significantly improved clinical outcomes in patients with acute ischemic stroke; alteplase was more frequently associated with symptomatic intracranial hemorrhage. (ClinicalTrials.gov number, NCT00153036.) 2008 Massachusetts Medical Society
              Article 0 comments Cited 797 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Liang Han
                Journal
                Journal ID (nlm-ta): Acta Pharm Sin B
                Journal ID (iso-abbrev): Acta Pharm Sin B
                Title: Acta Pharmaceutica Sinica. B
                Publisher: Elsevier
                ISSN (Print): 2211-3835
                ISSN (Electronic): 2211-3843
                Publication date PMC-release: 31 December 2020
                Publication date (Print): August 2021
                Publication date (Electronic): 31 December 2020
                Volume: 11
                Issue: 8
                Pages: 2306-2325
                Affiliations
                [a ]Jiangsu Key Laboratory of Neuropsychiatric Diseases Research, College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China
                [b ]Key Laboratory of Smart Drug Delivery, Ministry of Education, State Key Laboratory of Medical Neurobiology, Department of Pharmaceutics, School of Pharmacy, Fudan University, Shanghai 200032, China
                Author notes
                [∗ ]Corresponding author. Tel./fax: +86 512 65882089. hanliang@ 123456suda.edu.cn
                Article
                Publisher Item ID: S2211-3835(20)30852-2
                DOI: 10.1016/j.apsb.2020.11.023
                PMC ID: 8424230
                PubMed ID: 34522589
                SO-VID: 74e9304d-004c-454d-8878-f84fbcac83ab
                Copyright © © 2021 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 17 August 2020
                Date revision received : 30 September 2020
                Date accepted : 9 October 2020
                Categories
                Subject: Review

                Keywords: blood–brain barrier,brain diseases,brain-targeting,drug delivery systems,nanoparticles,aβ, amyloid beta,ad, alzheimer's disease,amt, alpha-methyl-l-tryptophan,bace1, β-secretase 1,bbb, blood–brain barrier,bdnf, brain derived neurotrophic factor,btb, blood–brain tumor barrier,cmt, carrier-mediated transportation,dtpa-gd, gd-diethyltriaminepentaacetic acid,epr, enhanced permeability and retention,gd, gadolinium,glut1, glucose transporter-1,icam-1, intercellular adhesion molecule-1,katp, atp-sensitive potassium channels,kca, calcium-dependent potassium channels,lat1, l-type amino acid transporter 1,ldl, low density lipoprotein,ldlr, ldl receptor,lfa-1, lymphocyte function associated antigen-1,lrp1, ldlr-related protein 1,mfsd2a, major facilitator superfamily domain-containing protein 2a,mmp9, metalloproteinase-9,mri, magnetic resonance imaging,nps, nanoparticles,pd, parkinson's disease,peg, polyethyleneglycol,peg-plga, polyethyleneglycol-poly(lactic-co-glycolic acid),p-gp, p-glycoprotein,plga, poly(lactic-co-glycolic acid),psma, prostate-specific membrane antigen,rage, receptor for advanced glycosylation end products,rbc, red blood cell,rmt, receptor-mediated transcytosis,ros, reactive oxygen species,sirna, short interfering rna,tbi, traumatic brain injury,tfr, transferrin receptor,tj, tight junction,tpa, tissue plasminogen activator,vegf, vascular endothelial growth factor,zo1, zona occludens 1
                Data availability:
                Keywords: blood–brain barrier, brain diseases, brain-targeting, drug delivery systems, nanoparticles, aβ, amyloid beta, ad, alzheimer's disease, amt, alpha-methyl-l-tryptophan, bace1, β-secretase 1, bbb, blood–brain barrier, bdnf, brain derived neurotrophic factor, btb, blood–brain tumor barrier, cmt, carrier-mediated transportation, dtpa-gd, gd-diethyltriaminepentaacetic acid, epr, enhanced permeability and retention, gd, gadolinium, glut1, glucose transporter-1, icam-1, intercellular adhesion molecule-1, katp, atp-sensitive potassium channels, kca, calcium-dependent potassium channels, lat1, l-type amino acid transporter 1, ldl, low density lipoprotein, ldlr, ldl receptor, lfa-1, lymphocyte function associated antigen-1, lrp1, ldlr-related protein 1, mfsd2a, major facilitator superfamily domain-containing protein 2a, mmp9, metalloproteinase-9, mri, magnetic resonance imaging, nps, nanoparticles, pd, parkinson's disease, peg, polyethyleneglycol, peg-plga, polyethyleneglycol-poly(lactic-co-glycolic acid), p-gp, p-glycoprotein, plga, poly(lactic-co-glycolic acid), psma, prostate-specific membrane antigen, rage, receptor for advanced glycosylation end products, rbc, red blood cell, rmt, receptor-mediated transcytosis, ros, reactive oxygen species, sirna, short interfering rna, tbi, traumatic brain injury, tfr, transferrin receptor, tj, tight junction, tpa, tissue plasminogen activator, vegf, vascular endothelial growth factor, zo1, zona occludens 1

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