T-Tau is Associated with Objective Memory Decline Over Two Years in Persons Seeking Help for Subjective Cognitive Decline: A Report from the Gothenburg-Oslo MCI Study
Affiliations: [a] Department of Neurology, Akershus University Hospital, Oslo, Norway | [b] Clinical Neuroscience Research Group, Department of Psychology, University of Oslo, Oslo, Norway | [c] Institute of Neuroscience and Physiology, Sahlgrenska Academy at Gothenburg, University, Mölndal, Sweden | [d] Faculty of Medicine, University of Oslo, Oslo, Norway
Correspondence:
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Correspondence to: Erik Hessen, Department of Neurology, Akershus University Hospital, Norway. Tel.: +47 92097373; [email protected]
Abstract:
Background: There is a need to find very early markers for pre-clinical Alzheimer’s disease as interventions early in the disease process are thought to be most effective.
Objective: The present study aimed to address the potential relation between cerebrospinal fluid (CSF) biomarkers and reduced cognitive function in a relatively young cohort of memory clinic patients with subjective cognitive decline.
Methods: 122 patients (mean age 63 years) with subjective cognitive decline were recruited from two university memory clinics and followed for two years.
Results: The main finding was that the subgroup with objective memory decline during the study period had significantly higher T-tau at baseline than the group with improved memory. Baseline CSF variables showed a trend toward more pathological values in the patients with memory decline compared to those who improved or remained stable. The baseline memory score of those who declined was significantly better than the baseline score of those who improved over two years. The general trend for the whole group was improved memory and executive test scores. There were no differences in cognitive scores based on CSF quartiles at baseline, nor were there differences in cognitive outcome for patients with early amnestic mild cognitive impairment versus average cognitive function at baseline.
Conclusions: The main finding that T-tau rather than amyloid-β was associated with memory decline do not support the prevailing opinion about the chain of events assumed to take place in Alzheimer’s disease. In addition, memory decline was not associated with poor baseline memory score. Thus, a memory cut-off indicating low baseline memory would not would have identified the declining group.
