Although the mechanisms underlying apoE4's action in AD pathogenesis are still poorly understood, emerging data strongly suggest that apoE4 contributes to this disease by interacting with different factors through various pathways.
In order to clarify the role of the polymorphism for the occurrence of LOAD in Chinese and the possibility of a synergistic effect with the apolipoprotein E allele 4 on the risk of Alzheimer disease, we examined the ACE and APOE genotypes in a Chinese sample consisting of 104 sporadic LOAD patients and 128 healthy controls.
There was a significant interaction between cholesterol, APOE-epsilon4, and the risk of Alzheimer disease (AD) in the Yoruba, a population that has lower cholesterol levels and lower incidence rates of AD compared to African Americans.
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.
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.