Alzheimer's Disease Model

Introduction

Alzheimer's disease (AD), often referred to as senile dementia, is clinically characterized by persistent global intellectual disability, cognitive dysfunction, psychiatric and behavioral abnormalities, and the inability to live independently or work. Pathologically, the brains of affected patients exhibit plaque deposition between dying neurons, intracellular neurofibrillary tangles, and widespread atrophy of the hippocampus and other brain regions.

Disease models

The SMOC has long been dedicated to research on neurodegenerative diseases and has independently developed a series of mouse and rat models for Alzheimer's disease (AD), which can be used for exploring disease mechanisms or conducting pharmacological and efficacy studies.

Alzheimer's disease model in hAPPNL-G-F mice

Amyloid precursor protein (APP) is closely associated with Alzheimer's disease (AD), and the accumulation of β-amyloid protein (Aβ) derived from its proteolytic cleavage in the brain is a key factor in the pathogenesis of AD. Using ES cell targeting technology, SMOC partially replaced the mouse App gene with the human APPNL-G-F sequence, enabling the expression of a human-mouse chimeric APPNL-G-F protein. In these homozygous mice, significant plaque accumulation gradually develops in the brain with increasing age.

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Fig1. Detection of APP expression in brain by RT-PCR.

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Fig2. (A) β-Amyloid (6E10) staining of WT and hAPPNL-G-F mice at 1, 3 and 6 months (magnification, 40x and 100x). (B) Statistics of 6E10 positive plaque area.

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Fig3. (A) Thioflavine S staining of WT and hAPPNL-G-F mice at 1, 3 and 6 months (magnification, 40x and 100x). (B) Statistics of ThiS positive plaque area.

Alzheimer's Disease Model in 5XFAD Mice

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Mutations: APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V

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Fig 1. Expression of Aβ in brain of 6-month-old 5xFAD mice.

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Fig 2. ELISA analysis of CSF sample collected from 5xFAD mice for human Aβ42.

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Fig 3. Results of Aβ 6E10 and Iba1 immunocostaining in 5xFAD mice after 3 months of Lecanemab treatment (90mpk, Q2W; n=6, male; dosing started at 7w).

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Fig 4. Aβ 6E10 Area  fraction in cortex and hippocampis of 5xFAD mice after Lecanemab treatment.


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