Additionally, the role of specific mutations in familial Alzheimer's disease has been explored, with research identifying resistant and resilient mutations that may provide insights into protective mechanisms against the disease (ref: Sepulveda-Falla doi.org/10.1186/s13024-023-00626-3/). Another study examined the expression of GEMIN5, a protein critical for spliceosome assembly, revealing its regulatory relationship with SMN in neurodegenerative contexts, particularly in spinal muscular atrophy (SMA) (ref: Fortuna doi.org/10.1007/s00401-023-02607-8/). The association of psychotic symptoms with specific pathology types in frontotemporal dementia has also been documented, indicating that subtype B pathology correlates with greater TDP-43 burden in white matter (ref: Hirsch-Reinshagen doi.org/10.1111/nan.12921/). These findings highlight the complexity of neurodegenerative diseases, where genetic, environmental, and pathological factors converge, necessitating a multifaceted approach to research and treatment.