Researchers from Australia have come to the conclusion that a high risk genotype that raises the chances for Alzheimer's disease, does not add changes in the carrier, pertaining to communication skills and memory during most of their adulthood. Those with the high risk gene seem to get affected by dementia, only much later in old age, along with other factors.
The study, has been described as the largest of its kind. This research unearthed that both carriers and non-carriers seem to age normally in the same pattern with similar decline in cognitive function over the years. Decades later, carriers show up with symtoms of aging that begin to snowball into pronounced symptoms of dementia. The findings imply that the genotype which promotes risk of developing this degenerative disorder plays a role much later. The findings are published in the January issue of Neuropsychology, by the American Psychological Association (APA).The study may help rule out the possibility of very early Alzheimer's as the cause of the decline among carriers before they reach old age,write the authors, "[Alzheimer's disease] processes may occur later in the lifespan and add to normal cognitive aging to produce a dementia syndrome." The study confirmed that carriers of the APOE4 gene type (allele), which confers higher risk for Alzheimer's, are just like other people their age throughout most of adult life in terms of core mental functions. Previous findings had been unclear. Lead author Anthony Jorm, PhD, DSc, explains, "Although some areas of cognitive decline begin from early adulthood onwards, this is not due – as some have speculated -- to very early Alzheimer's changes in the brain."
The APOE gene helps to transport cholesterol through the production of apolipoprotein E. People carry two copies of APOE, each being one of four APOE alleles. APOE4 raises Alzheimer's risk. In this study, researchers at the University of Melbourne and Australian National University assessed whether the small percentage (varying by ethnicity) of the population that carries at least one copy of APOE4 are cognitively different from non-carriers long before anyone shows signs of dementia.
The authors studied 6,560 people living in Canberra or neighboring Queanbeyan enrolled in the PATH Through Life Project, a long-term study of aging that assesses people in the age groups of 20-24, 40-44, and 60-64 years every four years for a period of 20 years. Jorm and his colleagues evaluated whether, in each age group, carriers of APOE4 (27 percent in their sample) were significantly different from non-carriers on tests of functions affected by Alzheimer's: episodic memory, working memory, mental speed, reaction time, and reading vocabulary.
Performance on all tests (except for reading vocabulary, which tends to hold up with age) declined across age groups, a sign of normal cognitive aging. However, APOE4 did not affect performance at any age. Thus the researchers conclude that at least between ages 20 and 64, people with APOE4 age normally in those central cognitive functions.
This finding suggests that APOE4 heightens the risk for Alzheimer's in old age through an additional, as-yet-unknown process that accelerates or intensifies normal changes, pushing them into the range of disease. Jorm provides an analogy. "In general, hair becomes thinner with age," he says. "However, there are some people who have an additional hereditary factor that makes them bald at an early age."
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