THE RELATIONSHIP BETWEEN CSF AMYLOID BETA CONCENTRATIONS AND FREE AND CUED RECALL PERFORMANCE AMONG PARTICIPANTS WITH AMNESTIC MILD COGNITIVE IMPAIRMENT

Abstract

Alzheimer's Disease (AD) is a neurodegenerative disease which typically presents with a specific episodic memory impairment. Although accumulation of hypertphosphoryllated tau is held responsible for the neurodegeneration and hence the symptoms of AD, recent research suggests that changes in amyloid-β (Aβ) 1−42 concentrations might also be related to memory performance. We aimed to investigate whether cerebro-spinal fluid (CSF) Aβ42 concentrations are related to free and cued recall performance among a group of patients with amnestic type MCI. The results that will be presented here are part of a still ongoing research project. Currently, we have 18 participants diagnosed with amnestic type MCI. All participants underwent an extended procedure involving neurological examination, multimodal neuroimaging, neuropsychological assessment, and lumbar puncture for CSF biomarkers. Free and Cued Selective Reminding Test was used as the principal measure to assess memory performance. The CSF Aβ42 concentrations of the sample ranged between 299 and 1377 pg/mL. Based on their Aβ concentration, we assigned the sample into two groups: low Aβ group (n=9) and high Aβ group (n=9). The cutoff value was 850 pg/mL. Then, 2 groups were compared with regard to their FCSRT scores. Significant intergroup differences were found with regard to total free recall performance. Specifically, high-amyloid group had significantly higher total free recall scores than low amyloid group (U= 14.00, p<.05). On the other hand, with respect to cue index scores, which an indicator of how each participant is able to benefit from cues, there was not a statistically significant difference between the two groups. Our initial results suggest that reduced CSF Aβ42 concentrations might interfere with free recall performance. The fact that no significant relationship was found with regard to cued recall (which is a specific feature of AD amnesia) might suggest that Aβ42-related amnesia is different from tau-related one, which disconnects entorhinal cortex from the hippocampal formation initially and hence gives rise to typical amnesia (hippocampal-type) that does not improve with cuing. Functional disconnections due to Aβ42 accumulation within a larger network, such as default mode (DMN) is likely to underline such a non-hypocampal-type memory deficit.