Background: The thalamus has been identified as an early site of Alzheimer’s disease (AD)pathology, but its functional trajectory relative to hippocampal degeneration and its specificity fordistinct cognitive domains remain incompletely characterised in large-scale longitudinal data.Objective: To test the Thalamic Filter Model prediction that thalamic hardware (filter layer)degrades before hippocampal hardware (memory buffer) across the AD spectrum, with thalamicintegrity specifically predicting executive function but not memory, language, or visuospatialdomains.Methods: Longitudinal structural MRI and diffusion tensor imaging (DTI) data were drawn fromthe Alzheimer’s Disease Neuroimaging Initiative (ADNI), encompassing 804 participants (222cognitively normal [CN], 391 mild cognitive impairment [MCI], 191 dementia) with 2,412longitudinal observations and 1,232 DTI observations. Thalamic volume, posterior thalamicradiation fractional anisotropy (PTR-FA), and hippocampal volume were extracted and comparedacross disease stages. Partial correlations examined the independent relationship between thalamicvolume and specific cognitive domains after controlling for hippocampal volume. APOE4 carriereffects were examined within each disease stage.Results: Thalamic volume showed monotonic, statistically significant decline across theCN→MCI→Dementia spectrum (F(2,801)=13.11, η²=0.032, Cohen’s d=0.61). PTR-FA declinedconcurrently (F(2,653)=8.90, d=0.73). Hippocampal volume showed a larger overall effect(d=1.15) but with decline concentrated at the MCI→Dementia transition rather than CN→MCI,consistent with filter-before-transmitter degradation. Thalamic volume independently predictedexecutive function (partial r=0.094, p=0.010) after controlling for hippocampal volume, with zeroindependent relationship with memory (partial r=0.011, p=0.78), language (partial r=0.019,p=0.61), or visuospatial domains (partial r=0.024, p=0.51). APOE4 specifically amplified thalamicatrophy at the MCI stage (d=−0.224, p=0.039) with null effects at CN and Dementia stages andnull hippocampal APOE4 effects at all stages.Conclusion: Thalamic filter hardware degrades before hippocampal memory hardware across theAD spectrum, specifically predicting executive function loss. APOE4 amplifies thalamic atrophyduring the transitional MCI vulnerability window. These findings identify a potential earlyintervention window targeting thalamic integrity, with implications for patient stratification inclinical trials.