Predicting cognitive decline and dementia?

Dementia News 74, June-July 2007

The June issue of Archives of Neurology reports an interesting paper on neuropsychological testing able to predict cognitive decline (Blacker et al). Blacker et al examined altogether 342 patients, 235 of which with mild cognitive impairment. Participants were followed for approximately 5 years measuring cognitive performance using 6 cognitive tests. The authors evaluated the neuropsychological measures that at baseline predicted time to progression from normal cognition to mild impairment and from mild impairment to diagnosis of Alzheimer's disease (AD).

The risk of progressing from normal to mild impairment was greater among those scoring less on tests of episodic memory. The apolipoprotein E (APOE) epsilon 2 allele decreased this risk. A lower score of the California Verbal Learning Test and an increased time to complete part B of the Trail Making test, indicating impairment of both episodic memory and executive function, were significant predictors of time to progression from mild impairment to a clinical diagnosis of AD. In the group of subjects with mild impairment the APOE epsilon4 allele increased the risk for AD, perhaps by changing the pacing of the progression.

The paper by Blacker et al raises several points of interest. In absence of validated biomarkers able to predict the individual risk for cognitive impairment or for progression to AD of people with mild impairment, the paper suggests an important correlation between selected neuropsychological tests and progression toward dementia. Of particular interest is the observation that the progression from mild impairment to AD diagnosis is predicted by tests of both episodic memory and executive function; this last observations drives the attention to the investigations of brain neurotransmitters and areas beyond just the cholinergic ones. It may be hypothesized, for example, that cortical-limbic dopaminergic areas, important for executive functions, may be involved, thus opening to novel targets for pharmacological interventions in selected patients preceding or paralleling those on cholinergic transmission. Moreover, if all this precedes measurable neurodegeneration and neuronal loss, that means that functional changes, possibly induced by amyloid or tau-protein, have to be searched for and investigated in addition to their neurotoxic properties.

prof. Stefano Govoni
Department of Experimental and Applied Pharmacology, University of Pavia, Italy

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