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Exploring a mathematical model for the kinetics of beta-amyloid molecular imaging probes through a critical analysis of plaque pathology.

Abstract：

:Amyloid plaques are highly heterogeneous in content, size, density, and macromolecular crowding, as they are composed of masses of fibrils and other cellular material. Given this target architecture, the aggregated microenvironment offers a unique imaging target for ligands and positron emission tomography (PET) molecular imaging probes (MIPs). In this work, we address how the heterogeneous microenvironment of a plaque and its evolution may affect the kinetic rate constant of PET MIPs. We argue that macromolecular crowding will result in anomalous diffusion within plaque regions. To account for anomalous diffusion within plaques, we propose a diffusion-limited ligand-receptor compartmental model. Given the current state of knowledge about the pathological progression of Alzheimer's disease (AD), the model's parameters may be a function of the pathological progression of AD, which could result in biased estimates of the true amyloid load. The bias may be partially overcome through evaluation in conjunction with other measures of AD progression including cerebral glucose metabolism rate, neuronal cell loss, and activated inflammatory presence.

journal_name

Mol Imaging Biol

journal_title

Molecular imaging and biology

authors

Shoghi-Jadid K,Barrio JR,Kepe V,Huang SC

doi

10.1007/s11307-006-0037-4

keywords:

subject

Has Abstract

pub_date

2006-05-01 00:00:00

pages

151-62

issue

3

eissn

1536-1632

issn

1860-2002

journal_volume

8

pub_type

杂志文章

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