Interactions between Amyloid-beta and Tau in Cerebrospinal Fluid of People with Mild Cognitive Impairment and Alzheimer's Disease
Abstract
Background: Despite the physiological sequestration of amyloid-beta (A beta) peptides by various carriers, interactions between peptides and protein tau appear to be pathological and involved in the development of Alzheimer's disease (AD). A recent study reported increased A beta-tau interactions in the neurons of AD patients.
Objective: We investigated the possibility that levels of A beta-tau complexes in cerebrospinal fluid could be a prospective biomarker of AD, with greater sensitivity and specificity than A beta(1-42), tau, or phospho-tau individually. Methods: By means of ELISA, we estimated levels of the complexes in 161 people (non-demented controls, people with mild cognitive impairment (MCI), probable AD or other types of dementia).
Results: We found significant reductions in levels in people with MCI due to AD (down to 84.5%) or with AD (down to 80.5%) but not in other types of dementia. The sensitivity of the new biomarker to AD was 68.6%, the specificity 73.3% (compared to controls) or 59.1-66.1% (compared to other types of dementia).
No significant correlations were observed between the complexes and the remaining biomarkers or between those and Mini-Mental State Examination score. Conclusion: We suppose that attenuated levels of complexes in cerebrospinal fluid reflect the accumulation of A beta bound to tau in AD neurons and that changes start many years before symptom onset, analogously to those in A beta(1-42), tau, or phospho-tau.
Unfortunately, these complexes are not a significantly better biomarker of AD than current biomarkers.