Cg. Gottfries et al., EARLY DIAGNOSIS OF COGNITIVE IMPAIRMENT IN THE ELDERLY WITH THE FOCUSON ALZHEIMERS-DISEASE, Journal of neural transmission, 105(8-9), 1998, pp. 773-786
In dementia disorders, it can be assumed that the pathological process
in the brain has been present for a long time. It is therefore of imp
ortance to have a preclinical or an early clinical diagnosis. Obviousl
y, vulnerability genes, such as ApoE-4, can be diagnosed preclinically
. As we have no treatment to offer patients with genetic risk factors,
genotyping for ApoE-4 is at present of no clinical use. Trained neuro
psychologists have today access to sensitive tests which reveal cognit
ive impairment before the disturbances reach the level of dementia. La
boratory investigations of cerebrospinal fluid have so far yielded no
great results. Tau protein appears to be the most sensitive marker, bu
t it is unspecific. Chromogranin A separates early onset from late ons
et Alzheimer's disease and seems to be a marker for synaptic degenerat
ion. Synaptotagmin was also found to be reduced in patients with early
onset Alzheimer's disease. Still we do not know, however, whether the
se proteins are early markers for degenerative processes in the brain.
Laboratory investigations of blood have not yielded markers of use in
early or differential diagnosis of dementia disorders. In a study at
our own institute, however, we found serum-homocysteine (S-HCY) to be
an early and sensitive marker for cognitive impairment. In patients wi
th dysmentia (mild cognitive impairment), no less than 39% had patholo
gical S-HCY levels, indicating insufficient 1-carbon metabolism.