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Chronic inflammation can increase Alzheimer's risk of APOE4 carriers

Peripheral chronic inflammation was linked to increased risks for Alzheimer's disease total and previous disease behavior among apolipoprotein E4 (…

Peripheral chronic inflammation was linked to increased risks for Alzheimer’s disease total and previous disease behavior among apolipoprotein E4 ( APOE4 ) repositories, reported researchers.

Defined as C-reactive protein (CRP) levels of 8, 9 or 10 mg / l, this low-grade inflammation was associated with an increased risk of Alzheimer’s disease only in persons wearing [AP45400] APOE4 especially in the absence of cardiovascular diseases (HR 6.63, 95% CI 1.80-24.50, P = 0.005) according to Wendy Qiu, MD, Doctor of Boston University of Medicine, and colleagues.

In addition, APOE4 carriers with chronic inflammation had an increased risk of prior disease behavior than APOE4 non-inflammatory carriers (HR 3.52, 95% CI 1

.27-9.75 , P = 0.009) reported in JAMA Network Open .

“Finding What Mediation Factors for APOE4 Increases Alzheimer’s Disease Risk Is Important To Develop Intervention And Prevention Of The Disease,” Qiu says in a statement. “Because many elderly have chronic low-quality inflammation after suffering from common diseases such as cardiovascular disease, diabetes, pneumonia and urinary tract infection, or after surgery, it could be effective to treat chronic systemic inflammation in APOE4 carrier for Alzheimer’s dementia. “

The findings are consistent with those of Alzheimer’s disease models and recent human research, noted Keenan Walker, a doctor at Johns Hopkins School of Medicine, Baltimore, which was not involved in the study. 19659002]” It is becoming increasingly clear that inflammation is an important part of Alzheimer’s Disease Patient Physiology, “Walker told MedPage Today .” This study provides further evidence that low-quality systemic inflammation can act as a potent risk factor for Alzheimer’s disease development. “

In the study, Qiu group assessed data from 2,656 members of the Framingham Offspring Study (generation 2), a cohort of children from Framingham Heart Study. They defined chronic inflammatory status as at least two longitudinal serum CRP measurements above predetermined levels.

Patients were on average about 61 years at Their last CRP measurement. During 17 years of follow-up, 194 subjects developed dementia, of whom 152 had Alz domestic disease.

This phenomenon of Alzheimer’s Alzheimer’s disease and previous disease behavior in APOE4 carriers was not observed in APOE3 and APOE2 carriers with chronic low-grade inflammation. Although APOE2 carriers, higher levels of CRP with increasing age than APOE3 and APOE4 carriers, such as high CRP levels, were not bound to Alzheimer’s risk in

In a subset of study participants who had brain magnetic resonance formation (n = 1 761), APOE4 and chronic low grade inflammation associated with brain atrophy in the temporal lobe (beta = -0.88, SE 0.22 , P <0.001) and hippocampus (beta = -0.04, SE 0.01, P = 0.005).

“Our findings indicate that chronic low-grade inflammation interacts with APOE4 to accelerate the onset of Alzheimer’s disease in a pattern that depends on the CRP level,” noted Qiu and colleagues. “

” Because it is well documented that infection and inflammation are common in elderly people, and preclinical studies have reported that inflammation-induced Alzheimer’s disease pathological properties in mice that only bore APOE4 our results can explain why APOE4 ] carriers have an increased risk of Alzheimer’s disease at an old age and suggest that treatment of chronic low-grade inflammation may delay the onset of Alzheimer’s disease in APOE4 carriers, “they concluded.

Restrictions of the study include its lack of more frequent CRP assessments, its limited sample size for subassays and its inability as observation research to show o rsakssamband. The Framingham cohort lacks ethnic diversity and the results can not apply to non-white populations.

Funding for this study is provided by the National Heart, Lung and Blood Institute and with contributions from the National Institute of Neurological Disorders and Stroke and the National Institute on Aging. The researchers reported no conflicts of interest.

1969-12-31T19: 00: 00-0500

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