China bears a heavy burden of AD costs, which greatly change the estimates of AD cost worldwide.

A notably higher prevalence of dementia and AD was found in rural areas than in urban ones, and education might be an important reason for the urban-rural differences.

436Early-onset familial Alzheimer's disease (EOFAD) is a condition characterized by dementia onset at a relatively young age (before 65 years of age) and a positive family history for dementia. Multiple terminologies such as familial Alzheimer's disease (FAD) 1 , early-onset AD (EOAD) 2 , autosomal dominant AD (ADAD), and autosomal dominant forms of early-onset AD (ADEOAD) 3 have been used to describe similar but overlapping entities. We summarize the complex nosology in Figure 1.Diagnostic criteria have a tremendous impact on the EOFAD epidemiology. If we use the stringent criteria of EOAD as onset of disease at age＜61 years, and ADEOAD as occurrence of EOAD in at least three generations, the prevalence of EOAD and ADEOAD are 41.2 and 5.3 per 100,000 persons, respectively. 3This variable nosology poses a substantive challenge in identifying cases that should undergo predictive genetic testing in asymptomatic individuals for mutations in one of the three identified Alzheimer's disease (AD)-related causal genes, since ABSTRACT: Early-onset familial Alzheimer's disease (EOFAD) is a condition characterized by early onset dementia (age at onset < 65 years) and a positive family history for dementia. To date, 230 mutations in presenilin (PS1, PS2) and amyloid precursor protein (APP) genes have been identified in EOFAD. The mutations within these three genes (PS1/PS2/APP) affect a common pathogenic pathway in APP synthesis and proteolysis, which lead to excessive production of amyloid β. Compared with sporadic Alzheimer's disease (AD), EOFAD has some distinctive features including early age at onset, positive familial history, a variety of non-cognitive neurological symptoms and signs, and a more aggressive course. There is marked phenotypic heterogeneity among different mutations of EOFAD. Studies in presymptomatic mutation carriers reveal biomarkers abnormalities. EOFAD diagnosis is based on clinical and family history, neurological symptoms and examination, biomarker features, as well as genotyping in some cases. New therapeutic agents targeting amyloid formation may benefit EOFAD individuals. RÉSUMÉ: La maladie d'Alzheimer familiale à début précoce. La maladie d'Alzheimer familiale à début précoce (MAFDP) est une maladie caractérisée par une démence à début précoce (âge de début < 65 ans) et une histoire familiale de démence. À ce jour, 230 mutations dans les gènes des présélinines (PS1, PS2) et du précurseur de la protéine amyloïde (APP) ont été identifiées dans la MAFDP. Des mutations de ces 3 gènes (PS1, PS2, APP) touchent une voie pathogène commune dans la synthèse et la protéolyse de l'APP, ce qui entraîne la production excessive de protéine β-amyloïde. La MAFDP comporte des caractéristiques distinctes de la MA sporadique, dont un âge de début précoce, une histoire familiale positive, des symptômes et des signes neurologiques non cognitifs variés et une évolution plus rapide de la maladie. Il existe beaucoup d'hétérogénéité phénotypique parmi les différentes mutations dans la MAFDP. Des études effectuées ch...

The prevalence of MCI in elderly Chinese is higher in rural than in urban areas. Vascular-related MCI (MCI-CVD and MCI-VRF) was most common.

Over the 6-month treatment period, NBP was effective for improving cognitive and global functioning in patients with subcortical vascular cognitive impairment without dementia and exhibited good safety.