The fact that the allele epsilon 4 of the Apolipoprotein E (APOE) gene could act like a risk factor not only in late-onset familial and sporadic Alzheimer's disease (AD) but also in cerebrovascular disease (CVD) and vascular dementia (VaD) is still controversial.
The apolipoprotein E (APOE) epsilon 4 allele is known to influence risk of AD but it has been difficult to establish whether it affects episodic memory differently from other cognitive functions.
The objective was to evaluate the effects of the apolipoprotein E (ApoE) genotype and gender on the response to donepezil treatment in Alzheimer's disease.
We have previously reported the isoform-specific interaction of native human apolipoprotein E (APOE, gene; apoE, protein) epsilon 3 with the amyloid-ss peptide, Ass(1-40), the major component of the cerebral amyloid deposits that appear to cause Alzheimer's disease.
To further investigate, we have analyzed association between the apolipoprotein E (apo E) and bleomycin hydrolase (BH) polymorphisms and three groups of elderly patients: control subjects (T) (n = 68), late-onset sporadic DTA patients (DTAst) (n = 65) and other non vascular neurodegerative diseases (MNDA) (n = 52).
The apoE4 allele is a major risk factor for late-onset familial and sporadic Alzheimer's disease (AD) and is associated with a poor outcome after brain injury.
We conclude that sequence variation in the BACE1 or BACE 2 gene is not a significant risk factor for AD; however, a combination of a specific BACE1 allele and APOE epsilon 4 may increase the risk for Alzheimer disease over and above that attributed to APOE epsilon 4 alone.
Although confirmation is required, these findings suggest that HFE mutations are associated with increased oxidative stress and Braak stage, and that HFE and APOE genotypes are different between AD patients, high pathology and low pathology controls.
The effect of the ApoE epsilon4 allele on recognition memory for olfactory and visual stimuli in patients with pathologically confirmed Alzheimer's disease, probable Alzheimer's disease, and healthy elderly controls.
Because the structural and biophysical properties of a protein determine how it functions under normal and abnormal conditions, apoE4, with its multiple cellular origins and multiple structural and biophysical properties, might contribute to the pathology of AD through several different mechanisms.
Neuron-specific proteolytic cleavage of apoE4 is associated with increased phosphorylation of tau and may play a key role in the development of AD-related neuronal deficits.