Some chronic viral infections could contribute to age-related cognitive decline

  • A longitudinal study confirms findings from cross-sectional studies that certain common viral infections are factors in age-related cognitive decline.

Growing research has implicated infections as a factor in age-related cognitive decline, but these have been cross-sectional (comparing different individuals, who will have a number of other, possibly confounding, attributes). Now a large longitudinal study provides more evidence that certain chronic viral infections could contribute to subtle cognitive deterioration in apparently healthy older adults.

The study involved 1,022 older adults (65+), who had annual evaluations for five years. It revealed an association between cognitive decline and exposure to several viruses: cytomegalovirus (CMV), herpes simplex (HSV 2), and the protozoa Toxoplasma gondii.

More specifically, the IgG levels for HSV-2 were significantly associated with baseline cognitive scores, while the IgG levels for HSV-2 (genital herpes), TOX (which has been much in the news in recent years for being harbored in domestic cats, and being implicated in various neurological disorders), and CMV (a common virus which unfortunately rarely causes symptoms), but not HSV-1 (the cold sore virus), were significantly associated with greater temporal cognitive decline that varied by type of infection.

More research is obviously needed to determine more precisely what the role of different infectious agents is in cognitive decline, but the findings do point to a need for a greater emphasis on preventing and treating infections. They also add to the growing evidence that age-related cognitive decline isn't 'normal', but something that occurs when other health-related factors come into play.

http://www.eurekalert.org/pub_releases/2016-02/uops-scv020416.php

Reference: 

Related News

A study involving mice lacking a master clock gene called Bmal1 has found that as the mice aged, their brains showed patterns of damage similar to those seen in Alzheimer's disease and other neurodegenerative disorders. Many of the injuries seemed to be caused by free radicals.

A new study involving 96 older adults initially free of dementia at the time of enrollment, of whom 12 subsequently developed mild Alzheimer’s, has clarified three fundamental issues about Alzheimer's: where it starts, why it starts there, and how it spreads.

Analysis of 5715 cases from the National Alzheimer's Coordinating Center (NACC) database has found that nearly 80% of more than 4600 Alzheimer's disease patients showed some degree of vascular pathology, compared with 67% of the controls, and 66% in the Parkinson's group.

The jugular venous reflux (JVR) occurs when the pressure gradient reverses the direction of blood flow in the veins, causing blood to leak backwards into the brain.

The

Following on from the evidence that Alzheimer’s brains show higher levels of metals such as iron, copper, and zinc, a mouse study has found that amyloid plaques in Alzheimer’s-like brains with significant neurodegeneration have about 25% more copper than those with little neurodegeneration.

An Italian study has found that a significant percentage of Alzheimer’s patients suffer from Obstructive Sleep Apnea Syndrome. This respiratory disorder, which causes people to temporarily stop breathing during their sleep, affects cerebral blood flow, promoting cognitive decline.

Data from 70 older adults (average age 76) in the Baltimore Longitudinal Study of Aging has found that those who reported poorer sleep (shorter sleep duration and lower sleep quality) showed a greater buildup of amyloid-beta plaques.

A new discovery helps explain why the “Alzheimer’s gene” ApoE4 is such a risk factor.

Analyses of cerebrospinal fluid from 15 patients with Alzheimer's disease, 20 patients with mild cognitive impairment, and 21 control subjects, plus brain tis

Pages

Subscribe to Latest newsSubscribe to Latest newsSubscribe to Latest health newsSubscribe to Latest news