Amyloid Beta Level in Serum Predicts Risk for Vascular Disease in First-Degree Relatives of Alzheimer’s Patients

People with a family history of Alzheimer’s disease, who have high levels of amyloid beta (Aβ) in the serum, are at increased risk for vascular disease.

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indicative of increased amyloid beta production due to genetic and/or other risk factors.

Manhasset, NY (Vocus) February 6, 2009

People with a family history of Alzheimer’s disease, who have high levels of amyloid beta (A²) in the serum, are at increased risk for vascular disease. These heightened A² levels may predict whether those without symptoms may progress towards dementia in years to come.

Michael Mullan, MD, and his colleagues at the Roskamp Institute in Sarasota, Fl., collaborated with statisticians at the London School of Hygiene and Tropical Medicine to see if elevated levels of A² in the blood in first-degree relatives of Alzheimer’s patients are associated with risk factors for vascular disease. Recent studies have shown that vascular disease is a major risk factor for Alzheimer’s. They recruited 197 local study subjects from the Alzheimer’s Disease Anti-Inflammatory Prevention Trial, which included unaffected family members, as well as 98 community elders in Florida. They studied the association of amyloid beta levels in serum with risk factors for vascular disease, including total cholesterol, LDL, HDL, systolic blood pressure, diastolic blood pressure and serum creatinine. They also looked at medications prescribed for vascular disease or the risk factors associated with vascular disease.

A² in serum is used as a marker to predict A² accumulation in the brain, which is one of the key pathologies of Alzheimer’s. In this study, the scientists found A² levels were significantly higher in first-degree relatives of Alzheimer’s patients, as compared with the elder community controls. The scientists say they suspect this elevation may be “indicative of increased amyloid beta production due to genetic and/or other risk factors.”

“These findings suggest that an increased risk of Alzheimer’s disease associated with family history may be mediated in part through the enrichment of individuals with vascular risk factors and may be reflective of pre-symptomatic Alzheimer’s disease pathology,” Dr. Mullan and his colleagues wrote.

In another stunning finding in the same issue of Molecular Medicine, scientists from Virginia Commonwealth University, Northwestern University, UCSF, UCLA, University of Pennsylvania, and University of North Carolina, identified a genetic signature for a hepatitis C virus-induced liver cancer, and different genetic handprints for cirrhosis caused by hepatitis C. They were able to use these genetic signatures to distinguish between pathological stages of liver cancer and early disease states, suggesting a way to diagnose this hepatocellular carcinoma earlier in the disease process.

Molecular Medicine is published by The Feinstein Institute for Medical Research, part of the North Shore-LIJ Health System. For more information on the study, visit http://www.molmed.org or contact Veronica J. Davis. Free podcasts from the latest issue of Molecular Medicine are also available on the journal’s web site and in iTunes.

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