ReviewCNS & neurological disorders drug targets2009
Clearance of amyloid-beta peptide across the blood-brain barrier: implication for therapies in Alzheimer's disease.
Review in CNS & neurological disorders drug targets, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 285 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
285 citing papers in PubMed, 1 synthesis or guideline pooled it, 552 citations in OpenAlex.
- Meta-analysis of genome-wide association studies identifies ancestry-specific associations underlying circulating total tau levels.Communications biology · 2022Pooled it
- The sleep-deprived blood-brain barrier: Does the Brain's gatekeeper adapt or merely fail slowly?Neurobiology of sleep and circadian rhythms · 2026Review
- Effects of HIV and azidothymidine on Alzheimer's-like pathology and amyloid beta transporters in hu-PBL-NSG mice, brain endothelial amyloid beta uptake and endothelial barrier integrity.Fluids and barriers of the CNS · 2026Article
- Intranasal Formaldehyde Exposure Induces RAGE-Mediated Alteration of the ADAM10/BACE1 Expression Balance and Amyloid Deposition.Biomedicines · 2026Article
- Article
- Plasma p-Tau217 and amyloid-β oligomers as complementary biomarkers for differential diagnosis, comorbidity detection and disease monitoring in idiopathic normal pressure hydrocephalus.Fluids and barriers of the CNS · 2026Article
- Reexamining the Role of Amyloid β Clearance from the Brain: Exporting Labile Iron from the Interstitial Fluid Performs a Protective Function.International journal of molecular sciences · 2026Review
- New insight into Alzheimer's disease: small molecule-Aβ in the brain transport and peripheral organ clearance.Frontiers in aging · 2026Review
- Glycogen synthase kinase-3 activation and dysregulation of amyloid transport receptors expression and shedding in HIV-induced Alzheimer's disease-like pathology: modulatory effects of CCR5 antagonists.Acta neuropathologica communications · 2025Article
- The integrity of perivascular spaces is absolutely essential for proper function of the glymphatic system waste and excess water removal from the brain.Histology and histopathology · 2025Review
- APOE4 Exacerbates Alzheimer-Like Pathologies and Cognitive Deficits Induced by Blood-Derived Aβ in a Mouse Model.Aging cell · 2025Article
- Angiopoietin signalling is a central axis of amyloid-driven vascular dysfunction in Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- The role of branched chain aminotransferase in the interrelated pathways of type 2 diabetes mellitus and Alzheimer's disease.Journal of diabetes and metabolic disorders · 2025Review
- Protective Effect of a Hexapeptide Derived from Rotifer-Specific SCO-Spondin Against Beta-Amyloid Toxicity.International journal of molecular sciences · 2025Article
- Endothelial progenitor cells and cerebral small vessel disease inCerebral circulation - cognition and behavior · 2025Article
- The pathophysiology of mixed Alzheimer's disease and vascular dementia.Theranostics · 2025Review
- The heart-brain axis: unraveling the interconnections between cardiovascular and Alzheimer's diseases.Frontiers in cardiovascular medicine · 2025Review
- Data-independent acquisition proteomic analysis of the brain microvasculature in Alzheimer's disease identifies major pathways of dysfunction and upregulation of cytoprotective responses.Fluids and barriers of the CNS · 2024Article
- Pathways to Alzheimer's Disease: The Intersecting Roles of Clusterin and Apolipoprotein E in Amyloid-β Regulation and Neuronal Health.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024Review
- Bioavailability as Proof to Authorize the Clinical Testing of Neurodegenerative Drugs-Protocols and Advice for the FDA to Meet the ALS Act Vision.International journal of molecular sciences · 2024Review
225 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The main receptors for amyloid-beta peptide (Abeta) transport across the blood-brain barrier (BBB) from brain to blood and blood to brain are low-density lipoprotein receptor related protein-1 (LRP1) and receptor for advanced glycation end products (RAGE), respectively. In normal human plasma a soluble form of LRP1 (sLRP1) is a major endogenous brain Abeta 'sinker' that sequesters some 70 to 90 % of plasma Abeta peptides. In Alzheimer's disease (AD), the levels of sLRP1 and its capacity to bind Abeta are reduced which increases free Abeta fraction in plasma. This in turn may increase brain Abeta burden through decreased Abeta efflux and/or increased Abeta influx across the BBB. In Abeta immunotherapy, anti-Abeta antibody sequestration of plasma Abeta enhances the peripheral Abeta 'sink action'. However, in contrast to endogenous sLRP1 which does not penetrate the BBB, some anti-Abeta antibodies may slowly enter the brain which reduces the effectiveness of their sink action and may contribute to neuroinflammation and intracerebral hemorrhage. Anti-Abeta antibody/Abeta immune complexes are rapidly cleared from brain to blood via FcRn (neonatal Fc receptor) across the BBB. In a mouse model of AD, restoring plasma sLRP1 with recombinant LRP-IV cluster reduces brain Abeta burden and improves functional changes in cerebral blood flow (CBF) and behavioral responses, without causing neuroinflammation and/or hemorrhage. The C-terminal sequence of Abeta is required for its direct interaction with sLRP and LRP-IV cluster which is completely blocked by the receptor-associated protein (RAP) that does not directly bind Abeta. Therapies to increase LRP1 expression or reduce RAGE activity at the BBB and/or restore the peripheral Abeta 'sink' action, hold potential to reduce brain Abeta and inflammation, and improve CBF and functional recovery in AD models, and by extension in AD patients.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.