Complies with the ATN criteria in clinical AD disease diagnosis A (Aβ): In the monkey model, cerebral Aβ deposition and aggregation progressively increase，while levels of CSF Aβ42 and Aβ42/Aβ40 ratio significantly decrease. T (Tau): In the monkey model, cerebral Tau deposition and aggregation progressively increase, and the level of CSF tTau significantly increases. N (Neurodegeneration): In the monkey model, elevated levels of NfL in CSF.

In the monkey model, continuous cognitive decline.

In the monkey model, neuroinflammatory signs appear in the gray and white matter of the prefrontal cortex, with activation of astrocytes (GFAP-positive) and microglia (Iba-1-positive).

Figure 1. WGTA test results revealed a significantly reduced correct response rate in the model monkeys, reflecting a notable impairment in cognitive function.

Figure 2. PET-CT imaging shows significant increases in Aβ and Tau deposition in the brains of AD model monkeys 2 months after modeling.

Figure 3. MSD results showed a significant decrease in cerebrospinal fluid Aβ42 and the Aβ42/Aβ40 ratio, and a significant increase in tTau and NfL in the model monkeys.

Figure 4. Immunohistochemistry using 4G8 and AT100 revealed significant Aβ plaques and Tau tangles in the cortex of the model monkeys.

Figure 5. Immunohistochemistry for GFAP and Iba1 revealed marked activation of astrocytes and microglia in the gray and white matter of the prefrontal lobe of the model monkeys.