Can mouse models mimic sporadic Alzheimer’s disease?

Alzheimer’s disease(AD)is a progressive neurodegenerative disorder and the most common form of dementia worldwide.As age is the main risk factor,>97%of all AD cases are of sporadic origin,potentiated by various risk factors associated with life style and starting at an age>60 years.Only<3%of AD cases are of genetic origin caused by mutations in the amyloid precursor protein or Presenilins 1 or 2,and symptoms already start at an age<30 years.In order to study progression of AD,as well as therapeutic strategies,mouse models are state-of-the-art.So far many transgenic mouse models have been developed and used,with mutations in the APP or presenilin or combinations(3×Tg,5×Tg).However,such transgenic mouse models more likely mimic the genetic form of AD and no information can be given how sporadic forms develop.Several risk genes,such as Apolipoprotein E4 and TREM-2 enhance the risk of sporadic AD,but also many risk factors associated with life style(e.g.,diabetes,hypercholesterolemia,stress)may play a role.In this review we discuss the current situation regarding AD mouse models,and the problems to develop a sporadic mouse model of AD.

Structural brain volume differences between cognitively intact ApoE4 carriers and non-carriers across the lifespan

Apolipoprotein E4（ApoE4） is a prominent genetic risk factor for Alzheimer＇s disease. The purpose of this review is to explore differences in structural brain volume detected by magnetic resonance imaging between cognitively intact ApoE4 carriers and non-carriers across the lifespan（i.e., older adults, middle-aged adults, young adults, children and adolescents, and neonates）. Consistent findings are found throughout various developmental stages. This area of research may elucidate the mechanisms by which ApoE4 influences risk of developing Alzheimer＇s disease. It could also inform potential treatment strategies and interventions for carriers of the ApoE4 allele.