Table 1.
Mechanism | WS1 | AD |
---|---|---|
ER stress | Chronic ER stress, apoptosis | Excessive UPR, neuronal death |
Calcium dysregulation | Dysregulated calcium signaling | Calcium influx, excitotoxicity |
Neurodegeneration | Neuronal death in the brainstem and cerebellum | Synaptic dysfunction, brain atrophy |
Aβ and Tau accumulation | Absent | Present (Aβ plaques, tau tangles) |
Overview of shared and distinct pathological mechanisms between WS1 and AD, highlighting similarities such as ER stress, calcium dysregulation, and neurodegeneration, as well as differences such as the absence of Aβ and Tau accumulation in WS1 [12].