Onset of cognitive impairment delayed among those heterozygous for the apolipoprotein E3 Christchurch variant<\/p>\n<\/h3>\n
By Elana Gotkine HealthDay Reporter<\/b><\/p>\n
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THURSDAY, June 20, 2024 (HealthDay News) — Cognitive impairment is delayed among persons who are heterozygous for the apolipoprotein E3 Christchurch variant (APOE3Ch<\/sup><\/em>), according to a study published in the June 20 issue of the New England Journal of Medicine<\/em>.<\/p>\n Yakeel T. Quiroz, Ph.D., from Massachusetts General Hospital in Boston, and colleagues analyzed data from 27 participants with one copy of the APOE3Ch<\/sup><\/em> variant among 1,077 carriers of the PSEN1E280A<\/sup><\/em> variant, which causes autosomal dominant Alzheimer disease, to estimate the age at onset of cognitive impairment and dementia.<\/p>\n The researchers found that the median age at onset of cognitive impairment was 52 years versus 47 years among carriers of PSEN1E280A<\/sup><\/em> who were heterozygous for the APOE3Ch<\/sup><\/em> variant compared with those without the APOE3Ch<\/sup><\/em> variant. 18<\/sup>F-fluorodeoxyglucose positron-emission tomographic imaging in two participants with PSEN1E280A <\/sup><\/em>and APOE3Ch<\/sup><\/em> variants showed relatively preserved metabolic activity in areas typically involved in Alzheimer disease. In one participant, tau findings were limited compared with persons with PSEN1E280A <\/sup><\/em>in whom cognitive impairment occurred at the typical age. Compared with autopsy material obtained from persons who had the PSEN1E280A<\/sup><\/em> variant but not the APOE3Ch<\/sup><\/em> variant, fewer vascular amyloid pathologic features were seen in persons with PSEN1E280A <\/sup><\/em>and APOE3Ch<\/sup><\/em> variants.<\/p>\n “The clinical, cognitive, neuroimaging, and neuropathological data that we present here provide evidence that APOE3Ch<\/sup><\/em> heterozygosity delayed the onset of cognitive impairment in a form of autosomal dominant Alzheimer’s disease and may have a protective effect against Alzheimer’s disease and neurodegeneration in this population,” the authors write.<\/p>\n Abstract\/Full Text (subscription or payment may be required)<\/a><\/p>\n Editorial (subscription or payment may be required)<\/a><\/p>\n <\/i><\/p>\n