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Cortex Area Thinner in Youth with Alzheimers-Related Gene

cations/UnravelingTheMystery/Part1/Hallmarks.htm">http://www.nia.nih.gov/Alzheimers/Publications/UnravelingTheMystery/Part1/Hallmarks.htm) characteristic of the disorder.

Previous studies had also implicated in Alzheimers one of three versions of a gene that produces ApoE. The ApoE4 variant occurs in 10-25 percent of the general population, but in 40 percent of late-onset Alzheimers patients. The strongest genetic risk factor for the disease discovered to date, ApoE4 has been linked to altered brain activity in adults and impaired neuronal development.

Shaw and colleagues suspected that youth with ApoE4 would have a thinner entorhinal cortex. To confirm this, they compared the MRI (magnetic resonance imaging) scans of 239 healthy children and teens with their ApoE gene types. Many were re-scanned as they grew up to see if there was any ongoing thinning process traceable to ApoE4.

Each individual inherits two copies of the ApoE gene, one from each parent. Youth with at least one copy of the relatively rare ApoE2 variant — which may confer a protective effect against developing Alzheimers — showed the thickest entorhinal cortex. This was the first evidence that the ApoE2 version, which is carried by 5-10 percent of the population, affects brain structure, say the researchers. Youth with two copies of ApoE3, the most common version (65-85 percent prevalence), had intermediate cortex thickness. Those with one or two copies of ApoE4 had the thinnest entorhinal cortex.

ApoE4 gene type also predicted thinning of two other brain regions (medial temporal and posterior orbitofrontal areas) affected early in Alzheimers disease, which, like the entorhinal cortex, are involved in learning and memory. The pattern of changes resembled that seen in early Alzheimers, but to a far lesser degree. For example, the entorhinal cortex thinning seen in Alzheimers disease is about 10-fold greater than in the youth with ApoE4.

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