Targeted Nanotherapy for Cognitive Impairment:  Blocking Amyloid-β-Induced Membrane Damage in Brain Tissue

Joseph D'Arrigo

doi:10.20944/preprints201808.0204.v1

Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Version 1 : Received: 9 August 2018 / Approved: 10 August 2018 / Online: 10 August 2018 (12:28:34 CEST)

A frequent co-morbidity of cerebrovascular pathology and Alzheimer's disease pathology has been observed over past decades. Accordingly, much evidence has been reported which indicates that microvascular endothelial dysfunction, due to cerebrovascular risk factors (e.g., atherosclerosis, obesity, diabetes, smoking, hypertension, aging), precedes cognitive decline in Alzheimer's disease and contributes to its pathogenesis. By incorporating appropriate drug(s) into biomimetic (lipid cubic phase) nanocarriers, one obtains a multitasking combination therapeutic which targets certain cell-surface scavenger receptors, mainly class B type I (i.e., SR-BI), and crosses the blood-brain barrier (BBB). Such targeting allows for various Alzheimer's-related cell types to be simultaneously searched out, in vivo, for localized drug treatment. This in vivo targeting advantage may be particularly important for repurposing an FDA-approved drug, especially one which has shown the added ability to restore some cognitive functions in certain animal models of Alzheimer's disease (e.g., the anticancer drug bexarotene); this (candidate repurposing) drug up to now, by itself (i.e, without nanocarrier), displayed poor CNS penetration in human subjects.

Alzheimer's disease; blood-brain barrier; cognitive aging; cognitive impairment; dementia; drug targeting; nanoemulsion; nanocarriers; scavenger receptors

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Targeted Nanotherapy for Cognitive Impairment: Blocking Amyloid-β-Induced Membrane Damage in Brain Tissue

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