To show that presymptomatic APOE epsilon4 homozygotes experience greater psychometric decline at a younger age than APOE epsilon4 heterozygotes and noncarriers before the diagnosis of mild cognitive impairment (MCI) and Alzheimer disease (AD).
Persons with higher age (OR 1.08, 95% CI 1.01-1.16), ApoE epsilon4 allele carriers (OR 2.04, 95% CI 1.15-3.64) and persons with medicated hypertension (OR 1.86, 95% CI 1.05-3.29) were more likely to convert to MCI than those individuals of lower age and without an ApoE epsilon4 allele or medicated hypertension.
The plasma protein apolipoprotein E (APOE) is a risk factor for degenerative cognitive decline manifested by mild cognitive impairment and later by Alzheimer's disease.
We present a random change point model to characterize decline in cognition among community-based elderly who developed Alzheimer's disease (AD) or amnestic mild cognitive impairment (MCI), and to examine how decline varies with age, sex, education, and APOE status.
Further, female APOE ε4 carriers showed a greater longitudinal reduction of HpVR than their male counterparts in the NC group, but not in the MCI or AD group.
Multiple logistic regression analysis identified a blunted nocturnal BP decline, non-dipping or increase in nocturnal BP and extreme drop in BP as potent determinants of MCI (odds ratio 3.062, P=0.039), after adjustment for possible confounding factors, including apolipoprotein E varepsilon4 genotype.
In addition, APOE methylation levels were significantly different between the MCI group and the control group (P = .021), especially in men (P = .006).
Since it is well established that the allele APOε4 is a major genetic risk factor for AD, we examined whether specific alleles of APOE could be associated with the different clinical outcomes between ASYMAD and MCI subjects despite equivalent AD pathology.
We observed a decrease in plasma Aβ40 and 42 among apolipoprotein E epsilon 4 (APOE ε4) carriers relative to noncarriers in the mild cognitive impairment trial.
To investigate whether APOE ε4 carriers have higher hippocampal atrophy rates than non-carriers in Alzheimer's disease (AD), mild cognitive impairment (MCI) and controls, and if so, whether higher hippocampal atrophy rates are still observed after adjusting for concurrent whole-brain atrophy rates.
Decreased CSF Abeta42 and elevated Tau or phospho-Tau together with APOE epsilon4 allele are highly predictive for the dementia in MCI patients with amnestic or executive symptoms.
Those with mild cognitive impairment (MCI) had an increased prevalence of the APOE4 allele, impaired performance on tests of memory, measures of IQ and naming compared to controls.
These results suggest that MRI measures of medial temporal atrophy, ApoE-ɛ4 genotype, and the protective effects of higher CR all predict the time to onset of symptoms associated with MCI in a largely independent, additive manner during the preclinical phase of Alzheimer's disease.
We included 115 participants from the Alzheimer's Disease Neuroimaging Initiative across the non-demented AD spectrum- defined as those who had at least one AD risk marker at baseline (e.g., mild cognitive impairment (MCI) due to AD diagnosis, amyloid or ApoE4 positivity) and/or 'cognitively normal individuals who converted to MCI due to AD or AD, with structural and diffusion tensor imaging scans at baseline and two years follow-up.
The APOE-ε4 allele was not associated with a diagnosis of cognitive impairment in PD (PD with mild cognitive impairment and PD with dementia) or with deficits in specific neuropsychological domains in our study cohort.
Over half of the AD and MCI subjects carried the ApoE4 (apolipoprotein E4) gene, which increases risk for AD; they showed greater hippocampal and temporal lobe deficits than non-carriers.
To evaluate cognitive performance and presence of polymorphisms of the genes SORL1(rs11218304), PVRL2(rs6859), CR1(rs6656401), TOMM40(rs2075650), APOE (isoforms ɛ2, ɛ3, ɛ4), PICALM(rs3851179), GWAS_14q(rs11622883), BIN1(rs744373), and CLU (rs227959 and rs11136000) in patients with MCI and healthy individuals.
The presence of the APOE epsilon4 allele is associated with impaired memory functioning in both middle-aged and old subjects with MCI, although the memory function affected varies with age.
This study compared (i) ventricular enlargement after six months in subjects with MCI, AD and normal elderly controls (NEC) in a multi-centre study, (ii) volumetric and cognitive changes between Apolipoprotein E genotypes, (iii) ventricular enlargement in subjects who progressed from MCI to AD, and (iv) sample sizes for multi-centre MCI and AD studies based on measures of ventricular enlargement.
The combined model (Harrell's C = 0.82 [0.78-0.86]) was significantly superior to demographics (β = 0.100, <i>P</i> < .001), magnetic resonance imaging (β = 0.037, <i>P</i> = .011), and PET only models (β = 0.053, <i>P</i> = .003).The models can be used to calculate individualized risk, for example, a female MCI patient (age = 60, APOE ε4 positive, Mini-Mental State Examination = 25, hippocampal volume = 5.8 cm<sup>3</sup>, amyloid PET positive) has 35% (19-57) risk in one year and 85% (64-97) risk in three years.
Possible joint effects of subjective cognitive decline (SCD) and apolipoprotein E (<i>APOE</i>) ε4 genotype on incident mild cognitive impairment (MCI) were examined for men and women separately.
Fibrillar Abeta was significantly associated with APOE epsilon4 carrier status and epsilon4 gene dose in AD-affected mean cortical, frontal, temporal, posterior cingulate-precuneus, parietal, and basal ganglia ROIs, and was highest in an additional homozygote who had recently developed mild cognitive impairment.