Abstract

Clinical symptoms and pathophysiological process of Alzheimer's Disease (AD) could be conceptualized as a continuum or trajectory. While change in amyloid-β (Aβ) 1−42 concentration in cerebrospinal fluid, which is thought to be the earliest pathophysiological process of AD trajectory, the earliest and core symptom of typical AD is generally an impairment in episodic memory. These changes are specific and sensitive predictive factors for people converting from mild cognitive impairment (MCI) and subjective cognitive impairment (SCI) to AD dementia. The aim of this study is to investigate how CSF Aβ1−42 concentration is related to free and cued recall and other cognitive functions in MCI and SCI. Our sample included 18 amnestic type MCI patients and 19 individuals with SCI. All participants underwent a multisession study including lumbar puncture and neuropsychological assessment. We used Free and Cued Selective Reminding Test to evaluate free and cued recall performance. These data were taken from an ongoing large study. Initial findings revealed that, compared to SCI group, MCI patients had lower scores on both free recall and cue index (t= 7.803 and 4.480, p<.05). Both free and cued recall were correlated to different measures of executive functioning and language (naming) (r values ranged between .46 and .65, p<.05) within SCI and MCI groups. In addition, among participants with MCI, lower CSF Aβ concentration was significantly related to worse free recall performance (r=.67, p<.05). As expected, there was no relationship between performance of recalling from cues and Aβ concentration within this group. Preliminary results revealed a significant relationship between higher Aβ pathology and free recall impairment within MCI group. On the other hand, cued recall impairment, which is a hallmark feature of AD, was not associated with Aβ pathology. Neither of the memory scores correlated with amyloid concentration among participants with SCI. It might be the case that in the continuum of AD, memory performance first interacts with executive functioning and language, and later with Aβ pathology in the CSF before the decrease of Aβ1–42 reaches a plateau.

Full Text
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