Genetic Alterations Contribute to Cognitive Decline in Alzheimer’s Patients

For some Chinese Alzheimer’s disease patients, genes can have an impact on cognitive decline. A recent study from Beijing Hospital & Beijing Institute of Geriatrics, Ministry of Health, entitled “APOE and APOC1 Gene Polymorphisms Are Associated with Cognitive Impairment Progression in Chinese Patients with Late-Onset Alzheimer’s Disease,” described the impact of specific genetic alterations on cognitive impairment progression for a subset of Alzheimer’s patients.

In total, 78 Chinese Han patients with late-onset Alzheimer’s disease from Guangxi Zhuang Autonomous Region in China were followed for 30 months. At the beginning of the study, patients were screened for genetic alterations in the genes encoding apolipoprotein E (APOE), apolipoprotein C1 (APOC1), and low density lipoprotein receptor-related protein (LRP). Throughout the longitudinal study, patients were assessed for cognitive function using the Mini-Mental State Examination (MMSE) and the Clinical Dementia Rating (CDR) Scale.

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Throughout the study, patients showed a reduction in MMSE total score, and more patients fulfilled the criteria for cognitive impairment. Patients who were identified to carry the APOE ε4 alteration were more likely to be cognitively impaired than not. Within this group, patients with the APOC1 H2 alteration were especially susceptible to cognitive decline. As a consequence, the researchers, led by Drs. Qin Zhou and Ze Yang, suggested that the two alterations together further increase the risk for cognitive decline in Chinese Alzheimer’s patients.

The role of apolipoproteins in Alzheimer’s disease may originate from the ability of APOE protein to bind to amyloid-beta, a protein notoriously associated with Alzheimer’s disease. In fact, the APOE genotype is widely accepted to raise the risk for Alzheimer’s disease. Research within the last few years has suggested that APOC1 and LRP also play a role in Alzheimer’s disease, motivating the basis for this study.