Aim: We aimed toevaluatethe psychometric properties of the Subjective Memory Complaints Questionnaire (SMCQ). Methods: The reliability of the SMCQ was evaluated by testing its internal consistency and test-retest reliability. Pearson correlation analyses were performed to assess the concurrent validity. Confirmatory factor analysis was used to evaluate the construct validity. Diagnostic ability for dementia was tested with receiver operator characteristic curve analyses. Results: Cronbach’s α coefficient and intraclass correlation coefficients of the SMCQ were 0.864 and 0.828 (p < 0.001), respectively. The SMCQ scores were significantly correlated with the scores on Camdex Memory Complaint Questionnaire, Seoul Informant Report Questionnaire for Dementia and cognitive tests from the CERAD (Consortium to Establish a Registry for Alzheimer’s Disease) neuropsychological test battery (p < 0.01). The results of confirmatory factor analyses confirmed that the SMCQ consisted of subjective memory complaints (SMC) for general memory and for everyday memory. The SMCQ score discriminated well between nondemented elderly without dementia and those with dementia (p < 0.01). The area under the curve value of the SMCQ was 0.84, indicating that it had high diagnostic ability. Conclusion: The SMCQ was found to be a brief, reliable and valid questionnaire for evaluating SMC. It might be useful for evaluating the cognition of elderly subjects when reliable informants are not available.

The study aimed to explore topographic progression pattern of brain functional impairment according to clinical stage in Alzheimer disease (AD). One hundred and sixteen AD patients and 25 normal subjects underwent a [¹⁸F] fluorodeoxyglucose-positron emission tomography scan. Regional cerebral glucose metabolism was compared between severity groups based on the Clinical Dementia Rating through voxel-based analyses. As clinical severity progressed, hypometabolic areas gradually increased, involving initially posterior cingulate cortex, later temporoparietal, and finally frontal and some subcortical areas. The results indicate that progression patterns of hypometabolism in AD are close to that of typical neuropathology, but that they do not fully coincide with it.

The Alzheimer’s disease (AD) pathology is characterized by fibrillar amyloid deposits and neurofibrillary tangles, as well as the activation of astrocytosis, microglia activation, atrophy, dysfunctional synapse, and cognitive impairments. The aim of this study was to test the hypothesis that astrocytosis is correlated with reduced gray matter density in prodromal AD. Twenty patients with AD or mild cognitive impairment (MCI) underwent multi-tracer positron emission tomography (PET) studies with ¹¹C-Pittsburgh compound B (¹¹C-PIB), ¹⁸ F-Fluorodeoxyglucose (¹⁸ F-FDG), and ¹¹C-deuterium-L-deprenyl (¹¹C-DED) PET imaging, as well as magnetic resonance imaging (MRI) scanning, cerebrospinal fluid (CSF) biomarker analysis, and neuropsychological assessments. The parahippocampus was selected as a region of interest, and each value was calculated for four different imaging modalities. Correlation analysis was applied between DED slope values and gray matter (GM) densities by MRI. To further explore possible relationships, correlation analyses were performed between the different variables, including the CSF biomarker. A significant negative correlation was obtained between DED slope values and GM density in the parahippocampus in PIB-positive (PIB + ve) MCI patients (p = 0.025) (prodromal AD). Furthermore, in exploratory analyses, a positive correlation was observed between PIB-PET retention and DED binding in AD patients (p = 0.014), and a negative correlation was observed between PIB retention and CSF Aβ42 levels in MCI patients (p = 0.021), while the GM density and CSF total tau levels were negatively correlated in both PIB + ve MCI (p = 0.002) and MCI patients (p = 0.001). No significant correlation was observed with FDG-PET and with any of the other PET, MRI, or CSF biomarkers. High astrocytosis levels in the parahippocampus of PIB + ve MCI (prodromal AD) patients suggest an early preclinical influence on cellular tissue loss. The lack of correlation between astrocytosis and CSF tau levels, and a positive correlation between astrocytosis and fibrillar amyloid deposition in clinical demented AD together indicate that parahippocampal astrocytosis might have some causality within the amyloid pathology.

Background: For the early detection of Alzheimer’s disease (AD), there is increasing interest in pre-mild cognitive impairment (pre-MCI). Objective: We explored the neuropsychological characteristics in a group of pre-MCI and cognitively normal (CN)