A specific capture carrier for removing β-amyloid protein and its application

Abstract

The invention belongs to the field of biotechnology, and specifically relates to a specific capture carrier for removing β-amyloid protein and its application. The specific capture carrier is specifically a functional nanoparticle, including: mesoporous silica nanoparticles, Ca‑MOF, Ce‑Mn MOF, mesoporous silica nanoparticles functionalized with anti-hAβ1‑42 monoclonal antibody, and mediators functionalized with anti-hAβ1‑42 monoclonal antibody and hyaluronic acid that can cross the blood-brain barrier Porous silica nanoparticles. These functional nanoparticles can rapidly clear Aβ1–42 in the blood and even the brain, and can reshape the distribution of Aβ in the intestine by changing the metabolic pathway of the antibody, thereby alleviating the disease process of neurodegenerative diseases such as Alzheimer’s disease, compared with the control group Compared with APP / PS1 mice intravenously injected with antibody-functionalized nanoparticles, β-amyloid protein in peripheral blood and brain was significantly reduced, and cecum and colon β-amyloid protein was significantly increased. It has potential application value in the treatment of silent disease.

Description

technical field [0001] The invention belongs to the field of biotechnology, and more specifically relates to a specific capture carrier for removing beta-amyloid protein and its application. Background technique [0002] β-amyloid (amyloid-β, Aβ) deposition is the key pathological basis of cerebral amyloid angiopathy (Cerebral amyloidangiopathy, CAA) and Alzheimer's disease (Alzheimer's disease, AD). Clinical data show that 80%-98% of AD patients are accompanied by cerebrovascular dysfunction and CAA, and the deposition of Aβ on the cerebrovascular wall is positively correlated with the severity and progress of the disease. AD is the most common neurodegenerative disease leading to dementia. Deposition of Aβ in the extracellular space of the cerebral cortex and in the walls of cerebral vessels is a hallmark of AD neuropathology. Current studies suggest that excess Aβ production or defects in Aβ clearance play a critical or pathogenic role in AD pathogenesis. AD includes f...

AI Technical Summary

Problems solved by technology

The latest research shows that Aβ also has similar transmission activity to prions, and Aβ from peripheral sources injected into the tail vein can enter and deposit in the brain of WT mice, inducing Aβ plaque aggregation and pro-inflammatory factors (TNF-α and IL-6) expression, leading to neuronal functional deficits

The above studies show the importance and feasibility of Aβ peripheral clearance, but pure Aβ antibody cannot achieve pure Aβ peripheral clearance

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