β-Amyloid (1-40), HFIP-treated, refers to the β-Amyloid (1-40) peptide that has been processed with HFIP. This peptide is a key protein fragment found in the brain plaques of individuals with Alzheimer's disease.

Before conducting formal experiments, it is advisable to determine optimal conditions (such as animal strain, age, dosage, frequency, duration, test times, and parameters) through preliminary tests. β-Amyloid (1-40) can be utilized in animal models to develop Alzheimer's disease models. The pathogenic mechanism involves β-Amyloid (1-40) accumulating in the brain with neurotoxic properties, thereby inducing Alzheimer's disease. Specific modeling method: Rats: Wistar • Male • 280-320 g Administration: 0, 3, 30, 300 pmol • Infusion using a cannula attached to a modified micro-osmotic pump • Duration: 2 weeks. Note: (1) Dissolve β-Amyloid (1-40) in 35% acetonitrile/0.1% trifluoroacetic acid (TFA). (2) Each group consists of 7 rats. On Day 1, insert the catheter into the left ventricle. Conduct the water maze task between days 9 and 13 after infusion begins. Post-behavioral experiments, decapitate 4 rats per group to measure ChAT activity, and use 3 rats for histochemical analysis. (3) For histochemical studies, anesthetize rats and euthanize them via transaortic perfusion fixation using cold saline followed by 4% paraformaldehyde and 0.1 M phosphate buffer. Extract and fix brains in the same fixative for 12 hours. Slice frozen brain tissue at 20 μm using a cryostat, collecting the periventricular region. Indicators of successful modeling include molecular changes: decreased acetylcholine transferase (ChAT) activity in the frontal cortex and hippocampus, leading to cholinergic neuron dysfunction; tissue changes: β-Amyloid accumulation in the hippocampus and cerebral cortex; and phenotypic observation: memory impairment.