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We examined whether cerebrovascular white matter pathology is related to cognition as measured by the compound score of CERAD neuropsychological battery in cognitively normal older adults, patients with mild cognitive impairment, and patients with Alzheimer's disease (total n = 149), controlling for age and education. Trend-level effects of white matter pathology on cognition were only observed in patients with Alzheimer's disease (p = 0.062, η2  = 0.052), patients with severe frontal white matter pathology performed notably worse than those with milder pathology. This indicates that frontal cerebrovascular pathology may have an additive negative effect on cognition in Alzheimer's disease.

Background: Atrophy of the deep gray matter (DGM) has been associated with a risk of conversion from mild cognitive impairment (MCI) to Alzheimer's disease (AD) and the degree of cognitive impairment. However, specific knowledge of the associations between degenerative DGM changes and neurocognitive functions remains limited., Objective: To examine degenerative DGM changes and evaluate their association with neurocognitive functions., Method: We examined DGM volume changes with tensor-based morphometry (TBM) and analyzed the relationships between DGM changes and neurocognitive functions in control (n = 58), MCI (n = 38), and AD (n = 58) groups with multiple linear regression analyses., Results: In all DGM areas, the AD group had the largest changes in TBM volume. The differences in TBM volume changes were larger between the control group and the AD group than between the other pairs of groups. In the AD group, volume changes of the right thalamus were significantly associated with episodic memory, learning, and semantic processing. Significant or trend-level associations were identified between bilateral caudate nucleus changes and episodic memory as well as semantic processing. In the control and MCI groups, very few significant associations emerged., Conclusions: Atrophy of the DGM structures, especially the thalamus and caudate nucleus, is related to cognitive impairment in AD. DGM atrophy is associated with tests reflecting both subcortical and cortical cognitive functions., (© 2019 S. Karger AG, Basel.)

Background: Type 2 diabetes (T2DM) increases the risk for Alzheimer's disease (AD) but not for AD neuropathology. The association between T2DM and AD is assumed to be mediated through vascular mechanisms. However, insulin resistance (IR), the hallmark of T2DM, has been shown to associate with AD neuropathology and cognitive decline., Objective: To evaluate if midlife IR predicts late-life cognitive performance and cerebrovascular lesions (white matter hyperintensities and total vascular burden), and whether cerebrovascular lesions and brain amyloid load are associated with cognitive functioning., Methods: This exposure-to-control follow-up study examined 60 volunteers without dementia (mean age 70.9 years) with neurocognitive testing, brain 3T-MRI and amyloid-PET imaging. The volunteers were recruited from the Finnish Health 2000 survey (n = 6062) to attend follow-up examinations in 2014-2016 according to their insulin sensitivity in 2000 and their APOE genotype. The exposure group (n = 30) had IR in 2000 and the 30 controls had normal insulin sensitivity. There were 15 APOEɛ4 carriers per group. Statistical analyses were performed with multivariable linear models., Results: At follow-up the IR+group performed worse on executive functions (p = 0.02) and processing speed (p = 0.007) than the IR- group. The groups did not differ in cerebrovascular lesions. No associations were found between cerebrovascular lesions and neurocognitive test scores. Brain amyloid deposition associated with slower processing speed., Conclusion: Midlife IR predicted poorer executive functions and slower processing speed, but not cerebrovascular lesions. Brain amyloid deposition was associated with slower processing speed. The association between midlife IR and late-life cognition might not be mediated through cerebrovascular lesions measured here.

Introduction: The educational background and size of the elderly population are undergoing significant changes in Finland during the 2020s. A similar process is likely to occur also in several European countries. For cognitive screening of early Alzheimer's disease (AD), using outdated norms and cutoff scores may negatively affect clinical accuracy. The aim of the present study was to examine the effects of education, age, and gender on the Consortium to Establish a Registry for Alzheimer's Disease neuropsychological battery (CERAD-nb) in a large register-based, clinical sample of patients with mild AD and nondemented at-risk persons from the general population (controls) and to examine whether corrected cutoff scores would increase the accuracy of differentiation between the 2 groups. Methods: CERAD-nb scores were obtained from AD patients (n = 389, 58% women, mean age 74.0 years) and from controls (n = 1,980, 52% women, mean age 68.5 years). The differences in CERAD-nb performance were evaluated by univariate GLM. Differentiation between the 2 groups was evaluated using a receiver operating characteristic (ROC) curve, where a larger area under the ROC curve represents better discrimination. Youden's J was calculated for the overall performance and accuracy of each of the measures. Results: Of the demographic factors, education was the strongest predictor of CERAD-nb performance, explaining more variation than age or gender in both the AD patients and the controls. Education corrected cutoff scores had better diagnostic accuracy in discriminating between the AD patients and controls than existing uncorrected scores. The highest level of discrimination between the 2 groups overall was found for two CERAD-nb total scores. Conclusions: Education-corrected cutoff scores were superior to uncorrected scores in differentiating between controls and AD patients especially for the highest level of education and should therefore be used in clinical cognitive screening, also as the proportion of the educated elderly is increasing substantially during the 2020s. Our results also indicate that total scores of the CERAD-nb are better at discriminating AD patients from controls than any single subtest score. A digital tool for calculating the total scores and comparing education-based cutoffs would increase the efficiency and usability of the test. [ABSTRACT FROM AUTHOR]

Concomitant white matter (WM) brain pathology is often present in patients with mild cognitive impairment (MCI) and Alzheimer's disease (AD). Cognitive effects of WM pathology on cognition in normal and pathological aging have been studied, but very little is known about possible group-specific effects in old age, MCI and AD. The purpose of the current study was to examine the relationship between WM pathology and cognitive functioning in four cognitive domains in old age, MCI and AD. The study utilized multi-domain neuropsychological data and visually rated MRI imaging data from a sample of 56 healthy older adults, 40 patients with MCI and 52 patients with AD (n = 148). After controlling for age and education, main effects of frontal WM pathology (especially in the left hemisphere) were found for cognitive performances in two domains, whereas a main effect of parieto-occipital WM pathology was only found for processing speed. In addition, with regard to processing speed, an interaction between group and WM changes was found: Patients with AD that had moderate or severe left frontal WM pathology were considerably slower than patients with AD that had milder cerebrovascular pathology. Frontal WM pathology, especially in the left hemisphere, seems to affect cognitive functions in many domains in all three groups. The results of the study increase our knowledge of cognitive repercussions stemming from frontal and/or parieto-occipital WM pathology in AD. Clinicians should be aware that patients with AD with prominent frontal cerebrovascular pathology can have considerably slowed cognitive processing. [ABSTRACT FROM AUTHOR]

We examined whether cerebrovascular white matter pathology is related to cognition as measured by the compound score of CERAD neuropsychological battery in cognitively normal older adults, patients with mild cognitive impairment, and patients with Alzheimer's disease (total n = 149), controlling for age and education. Trend-level effects of white matter pathology on cognition were only observed in patients with Alzheimer's disease (p = 0.062, η2  = 0.052), patients with severe frontal white matter pathology performed notably worse than those with milder pathology. This indicates that frontal cerebrovascular pathology may have an additive negative effect on cognition in Alzheimer's disease. [ABSTRACT FROM AUTHOR]

Emotional content is known to enhance memory in a content-dependent manner in healthy populations. In middle-aged and older adults, a reduced preference for negative material, or even an enhanced preference for positive material has been observed. This preference seems to be modulated by the emotional arousal that the material evokes. The neuroanatomical basis for emotional memory processes is, however, not well understood in middle-aged and older healthy people. Previous research on local gray matter correlates of emotional memory in older populations has mainly been conducted with patients suffering from various neurodegenerative diseases. To our knowledge, this is the first study to examine regional gray matter correlates of immediate free recall and recognition memory of intentionally encoded positive, negative, and emotionally neutral words using voxel-based morphometry (VBM) in a sample of 50-to-79-year-old cognitively intact normal adults. The behavioral analyses yielded a positivity bias in recognition memory, but not in immediate free recall. No associations with memory performance emerged from the region-of-interest (ROI) analyses using amygdalar and hippocampal volumes. Controlling for total intracranial volume, age, and gender, the whole-brain VBM analyses showed statistically significant associations between immediate free recall of negative words and volumes in various frontal regions, between immediate free recall of positive words and cerebellar volume, and between recognition memory of positive words and primary visual cortex volume. The findings indicate that the neural areas subserving memory for emotion-laden information encompass posterior brain areas, including the cerebellum, and that memory for emotion-laden information may be driven by cognitive control functions. [ABSTRACT FROM AUTHOR]

Background: Free recall memory deficits are common in Parkinson's disease (PD), even at early stages before mild cognitive impairment or dementia. Their association with brain structural changes has not been established. Objective: We studied local gray matter volumes in relation to different memory tasks in early stage PD. Methods: Magnetic resonance images (MRI) and neuropsychological data were obtained from 28 non-demented, medicated PD patients, and 28 healthy controls. The gray matter segments of T1-weighted MRI images were analyzed using voxel-based morphometry in relation to visual and verbal memory tasks. Measures of immediate free recall, verbal learning, delayed recall and memory consolidation were obtained. A novel measure of incidental memory was included. Results: Patients and controls showed no significant group differences in local gray matter volumes. Voxel-based morphometry analyses revealed that worse performance on an incidental visual memory task was associated with smaller right parietal gray matter volume (Family-wise error corrected P = 0.002). This association was present in the PD group (corrected P = 0.005), but not in controls (corrected P > 0.99). No associations between gray matter volumes and the other memory tasks were found in either group. Conclusions: The results suggest that right parietal cortical gray matter volume is related to free recall memory deficits in early stage PD in conditions not involving an intention to memorize visual items. This preliminary finding needs to be established in further studies utilizing incidental memory tasks in PD. [ABSTRACT FROM AUTHOR]

Abstract: Background: Frontostriatal and cognitive dysfunctions in Parkinson's disease (PD) are hypothesized to be linked predominately to dopaminergic dysfunction within neural networks linking dorsal striatum to dorsolateral prefrontal cortex. Methods: The authors evaluated the relationship between frontostriatal dopaminergic function and cognitive performance, especially cognitive processing speed by performing [18F]fluorodopa PET and computerized tests of automatic and controlled cognitive processing speed (CogniSpeed) in 23 newly diagnosed and unmedicated PD patients and 14 controls. Results: PD patients were slower than the controls in all the CogniSpeed measures studied. The Fdopa uptake in caudate nucleus correlated negatively with slowing on all the tests. Slower performance in relatively automatic processes measured by choice reaction tasks as well as in more controlled processes measured by a calculation task was related to reduced Fdopa uptake in the anterior cingulate gyrus. The reduced dopaminergic function in the thalamus was associated with the slower performance in the subtraction test. Conclusion: Our study indicates that dopaminergic dysfunction within neural networks linking striatum to prefrontal cortex is involved in the slowing of both automatic and controlled cognitive processing in PD patients. [Copyright &y& Elsevier]

Background/Aims: The relationship between baseline 11C-Pittsburgh compound B (11C-PIB) uptake and cognitive decline during a 2-year follow-up was studied in 9 patients with mild cognitive impairment (MCI) who converted to Alzheimer's disease (AD) and 7 who remained with MCI. Methods:11C-PIB PET scan was conducted at baseline and cognitive assessment both at baseline and at follow-up. To obtain quantitative regional values of 11C-PIB uptake, automated region of interest analysis was done using spatially normalized parametric ratio (region-to-cerebellar cortex) images. Results: At baseline, there were statistically significant differences in 11C-PIB uptake, but not in cognitive test performances between the converters and nonconverters. Memory and executive function declined only in the converters during follow-up. In the converters, lower baseline frontal 11C-PIB uptake was associated with faster decline in verbal learning. Higher baseline uptake in the caudate nucleus was related to faster decline in memory consolidation, and higher temporal uptake was associated with decline in executive function. Conclusion: Higher 11C-PIB uptake in the caudate nucleus and temporal lobe was related to decline in memory and executive functions, whereas lower frontal uptake was related to decline in verbal learning. The results indicate that in prodromal AD, frontal amyloid accumulation reaches its maximum in the MCI stage, characterized by memory problems without full-blown dementia. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]