When performing research studies comparing one group of subjects to another, stratification for age (and other demographic criteria) can be very valuable, in maintaining well-matched experimental and control groups. In comparing individual patients for clinical purposes, on the other hand -- where the goal is not to say how one group or condition compares to another, but rather what the metabolic images show in this individual's brain -- additional considerations pertain, and adjustments made for age can be quite misleading. For example, some individual healthy 70 year olds have brains with atrophy-related changes typical for someone 55 years old, while other healthy 70 year olds have brains with atrophy-related changes typical for someone 85 years old (this spectrum is something that is seen frequently.) In the context of the NeuroQ package, age stratification is not only unnecessary, but would actually be undesirable, for a number of reasons.
First, several published studies have shown (as reviewed in Radiologic Clinics of North America, 2005; 43:67-77) that in healthy aging, patterns of cerebral metabolism and perfusion demonstrate very little systematic change with age, and the one change that is consistently reported (in anteromedial prefrontal cortex) is distinct from changes that occur in the context of Alzheimer's and other neurodegenerative diseases.
Second, we have designed the NeuroQ display to visually represent that which is actually apparent in the primary PET scan data, and not give output that is distorted by diminished-sample statistical drifts, or models or assumptions about effects of aging. For example, when it is visually obvious that the medial prefrontal cortex is substantially decreased in the cerebral metabolism of an 80-year old, we want this to be reflected in the Program's color display rather than have the output appear all blue (as could occur if the output were age-adjusted). Moreover, since our normal database spans a wide age spectrum (20-89 years old), regions affected most by normal aging will have correspondingly larger SD's of normal variation, and this provides a built-in stabilization of the statistical component reflected in our two-dimensional (magnitude and statistical differences from the mean) color tool.
Third, since getting older is the single most powerful non-genetic predisposing factor for dementia, any attempt to age-adjust the database runs the risk of 'adjusting out' important information contained in the original scan. Except when the absence of early dementia-related changes are definitively proven (as rarely occurs) by autopsy (or very long-term clinical follow-up) of the 'normal' older patients, age adjustments may actually obscure metabolic data that are neurologically meaningful.