Alzheimer’s Disease, the most prevalent cause of dementia, is characterized by pathological deposition of toxic Amyloid-β plaques and presence of neurofibrillary tangles in the brain. Due to the multifactorial nature of this complex disease, no cure has been developed to address AD.

Familial Alzheimer’s disease (FAD) is a subtype of Alzheimer’s disease caused by autosomal dominant mutations. These mutations occur in the genes that code for amyloid precursor protein (APP) and the catalytic subunit of y-secretase complex, presenilin 1 (PSEN1) and presenilin 2 (PSEN2), accounting for less than 5% of all Alzheimer’s disease cases [1]. These gene mutations on APP, PSEN1 and PSEN2 lead to abnormal aggregation and deposition of toxic Amyloid-β plaques, which in turn cause the atrophy and death of neurons in cognitive-related brain regions, ultimately causing neurodegeneration and cognitive decline. Compared with sporadic Alzheimer’s disease, FAD has distinct characteristics. These include an earlier onset age (40-65 years old); faster progression (approximately 5 years from when symptoms appear to disability, which is 10-15 years shorter than in sporadic cases); and a clear mode of inheritance (50% probability of carrying the pathogenic mutation in first-degree relatives) [2]. Clinical symptoms often manifest as decline in episodic memory, decreased language fluency, abnormal visuospatial function, and comprehensive impairment of other cognitive functions, ultimately leading to loss of basic abilities and endangering the patient’s life. )