Does incipient dementia explain normal cognitive decline determinants? Lothian Birth Cohort 1921

The presence of an APOE ɛ4 allele, lower physical fitness, smoking, and lower serum vitamin B-12 have been reported as contributing to poorer cognitive function in LBC1921 at age 79, after adjusting for childhood intelligence. Because incident dementia was not previously ascertained within LBC1921, it is possible that preclinical or unrecognised cases at age 79 influenced findings. Dementia cases arising over approximately 16 years of follow-up were determined by a consensus using evidence from electronic medical records, death certificates, and clinical reviews. The analyses from the original reports were repeated following the exclusion of those who had developed dementia. In a subsequent set of analyses, the authors considered the potential impact of terminal decline, excluding those participants who died within four years of baseline testing. Positive APOE ɛ4 status was found to be associated with poorer Logical Memory (Wechsler, 1987) at age 79 (F1,355=8.16, p=0.005, ƞp2=0.022; n=359) and lower Moray House Test (Scottish Council for Research in Education, 1933) score at age 79 (F1,357= 4.27, p= 0.04, ƞp2 = 0.012; n=363). Lower age 79 IQ was associated with smoking (F2,360= 3.67, p=0.026, ƞp2=0.020; n=367), lower vitamin B-12 (Sβ=0.11, p=0.014; n=367), and poorer physical fitness (Sβ=0.21, p<0.001; n=359). Only the relationship with physical fitness remained significant after excluding those who died within 4 years of baseline (Sβ= 0.203, p<0.001; n=310). Unrecognised dementia had little or no effect on determinants of lifetime cognitive ageing in LBC1921. Terminal decline may have accounted for the associations with age 11 to age 79 cognitive change.