Damage to small blood vessels in the brain could be a secondary risk factor leading to Alzheimer’s Disease, a new study in JAMA Neurology suggests.

A part of this blood vessel damage is known as white matter hyperintensities, seen in the brains of Alzheimer’s patients and appearing to increase the risk for the disease, making it a secondary factor.

Experts believe the primary factor of Alzheimer’s development is the accumulation of beta amyloid plaques in the brain.

The study consisted of data from 20 subjects with Alzheimer’s Disease from the Alzheimer’s Disease Neuroimaging Initiative database, 59 participants with mild cognitive impairment, and data from 21 normal control subjects.

The authors discovered that both factors were independent predictors of Alzheimer’s disease.

Among participants with heightened amyloid plaque levels, those with Alzheimer’s had higher volumes of white matter hyperintensities or small brain lesions that were seen via MRI.

Among subjects with mild cognitive impairment, both factors predicted the development of Alzheimer’s disease.

The authors explained:

“White matter hyperintensities contribute to the presentation of Alzheimer’s disease and, in the context of significant amyloid deposition, may provide a second hit necessary for the clinical manifestation of the disease.”

Because some people remain cognitively healthy despite amyloidosis (the accumulation of beta-amyloid in the brain), the authors believe that amyloid deposition is needed to aid in the development of Alzheimer’s…….plus something else!

Researchers used MRI to establish the volume of white matter hyperintensities and PET studies with the Pittsburgh Compound B (PIB) tracer in order to quantify beta-amyloid positivity.

Among patients with Alzheimer’s disease and control subjects, 68 percent (28 scans) were categorized as PIB positive. Of this 68 percent, 11 were classified as normal control subjects and the rest as having Alzheimer’s disease.

Only three of the 13 without amyloidosis had the criteria for Alzheimer’s.

On average, the 59 participants with mild cognitive impairment were observed for 29.73 months. At the follow-up, 22 had progressed to Alzheimer’s disease.

During baseline, seven had low amyloid and low lesion volume, 17 had amyloidosis but low lesion volume, 11 had low amyloid but high lesion volume, and 24 were elevated in both factors.

The authors noted that across the four groups, those participants who progressed to Alzheimer’s at the follow-up increased steadily.

An implication of their findings could be that altering the risk factors for white matter hyperintensities could help prevent the clinical diagnosis of Alzheimer’s. However, the authors point out that this study is small and needs to be replicated in a larger population.

The researchers concluded, “It is becoming clear from studies such as this one and others that vascular factors are quite important in the pathogenesis of the (Alzheimer’s) phenotype.”

A recent study carried out by a team of researchers from UCLA suggests that vitamin D3 and omega 3 fatty acids can help the immune system rid the brain of amyloid plaques, a telltale sign of Alzheimer’s disease.

Written by Kelly Fitzgerald