Impairment of ADL is already present in MCI. Therefore, intact ADL cannot be used as a criterion to define the syndrome of MCI and to distinguish it from mild dementia. The assessment of complex ADL is probably useful for the diagnosis of MCI.
MCI patients may be impaired in complex ADL.
Reserve in aging and Alzheimer’s disease (AD) is defined as maintaining cognition at a relatively high level in the presence of neurodegeneration, an ability often associated with higher education among other life factors. Recent evidence suggests that higher resting-state functional connectivity within the frontoparietal control network, specifically the left frontal cortex (LFC) hub, contributes to higher reserve. Following up these previous resting-state fMRI findings, we probed memory-task related functional connectivity of the LFC hub as a neural substrate of reserve. In elderly controls (CN, n = 37) and patients with mild cognitive impairment (MCI, n = 17), we assessed global connectivity of the LFC hub during successful face-name association learning, using generalized psychophysiological interaction analyses. Reserve was quantified as residualized memory performance, accounted for gender and proxies of neurodegeneration (age, hippocampus atrophy, and APOE genotype). We found that greater education was associated with higher LFC-connectivity in both CN and MCI during successful memory. Furthermore, higher LFC-connectivity predicted higher residualized memory (i.e., reserve). These results suggest that higher LFC-connectivity contributes to reserve in both healthy and pathological aging.
BackgroundRecent evidence derived from functional magnetic resonance imaging (fMRI) studies suggests that functional hubs (i.e., highly connected brain regions) are important for mental health. We found recently that global connectivity of a hub in the left frontal cortex (LFC connectivity) is associated with relatively preserved memory abilities and higher levels of protective factors (education, IQ) in normal aging and Alzheimer’s disease. These results suggest that LFC connectivity supports reserve capacity, alleviating memory decline. An open question, however, is why LFC connectivity is beneficial and supports memory function in the face of neurodegeneration. We hypothesized that higher LFC connectivity is associated with enhanced efficiency in connected major networks involved in episodic memory. We further hypothesized that higher LFC-related network efficiency predicts higher memory abilities.MethodsWe assessed fMRI during a face-name association learning task performed by 26 healthy, cognitively normal elderly participants. Using beta-series correlation analysis, we computed task-related LFC connectivity to key memory networks, including the default mode network (DMN) and dorsal attention network (DAN). Network efficiency within the DMN and DAN was estimated by the graph theoretical small-worldness statistic. We applied linear regression analyses to test the association between LFC connectivity with the DMN/DAN and small-worldness of these networks. Mediation analysis was applied to test LFC connectivity to the DMN and DAN as a mediator of the association between education and higher DMN and DAN small-worldness. Last, we tested network small-worldness as a predictor of memory performance.ResultsWe found that higher LFC connectivity to the DMN and DAN during successful memory encoding and recognition was associated with higher small-worldness of those networks. Higher task-related LFC connectivity mediated the association between education and higher small-worldness in the DMN and DAN. Further, higher small-worldness of these networks predicted better performance in the memory task.ConclusionsThe present results suggest that higher education-related LFC connectivity to key memory networks during a memory task is associated with higher network efficiency and thus enhanced reserve of memory abilities in aging.Electronic supplementary materialThe online version of this article (10.1186/s13195-018-0358-y) contains supplementary material, which is available to authorized users.
Mild cognitive impairment (MCI) is often a prodromal state of Alzheimer's disease (AD). Imaging studies have shown that metabolic deficits in cerebral regions known to be affected early by AD pathology are predictive of progression to AD. In the present article, the authors examine associations between clinical impairment (Clinical Dementia Rating scale sum of boxes [CDR-SB]) and regional deficits in glucose utilization in a sample of 41 patients with MCI, who underwent cerebral 18F-FDG PET for the measurement of regional glucose metabolism. A linear regression analysis with CDR-SB score as the independent variable and glucose metabolism as the dependent variable, adjusted for age, gender, and years of school education, was conducted in voxel-by-voxel fashion in SPM2. The regression analysis revealed a significant negative association between CDR-SB score and glucose metabolism in the right posterior cingulate gyrus (P < .001, uncorrected for multiple comparisons), which was independent from demographical variables. The authors conclude that clinical severity of impairments is already correlated with deficits in glucose metabolism in the stage of MCI.
According to the diagnostic consensus criteria [1] akinesia, rigidity and tremor as well as primitive reflexes and incontinence support the diagnosis of fronto-temporal dementia (FTD). However, the prevalence of extrapyramidal signs (EPMS), primitive reflexes and incontinence in FTD has not yet been systematically studied. In the present study, thirty-one patients with mild or moderate FTD without previous or present antipsychotic medication underwent a detailed neurological exam including the motor part of the Unified Parkinson's Disease Rating Scale (UPDRS). The average total score on the motor subscale of the UPDRS was 14.0 points. Akinesia and Parkinsonian gait or posture were found frequently but were mild in most instances. Rigidity was found in 36% of the patients. Resting tremor was a rare symptom. The only primitive reflex that occurred was a positive palmomental that was found in 7% of the patients. Urinary incontinence was present in 26%. The results have to be confirmed with larger or pooled patient samples from different ascertainment scenarios. If the results of the present study can be replicated, a revision of the consensus criteria from 1998 might be considered.
The early and differential diagnosis of the clinical phenotypes of frontotemporal lobar degeneration (FTLD), including frontotemporal dementia (FTD), semantic dementia (SD) and non-fluent progressive aphasia (NFPA), can be challenging. It may be difficult not only to differentiate these conditions from normal aging, psychiatric disorders, and other dementias, but also to distinguish between them. For early diagnosis, information on the initial and presenting symptoms of the FTLD phenotypes is essential. In the present study caregivers of 78 patients with FTD, 20 patients with SD and 17 patients with PA were interviewed about initial symptoms. In patients with FTD, the most frequent initial symptoms were alterations of personality, followed by forgetfulness and word finding difficulty. Patients with SD presented with word finding difficulty and behavioral disturbances. Almost all patients with PA developed word finding difficulty as the first manifestation of their disorder. Diagnostic latency - the time from disease onset to diagnosis was 4.1 years in FTD, 4.2 years in SD and 3.1 years in PA. Caregivers, and in some cases also patients, should be educated about the likely course and mortality of FTLD. To obtain information about survival time and cause of death associated with FTLD we analyzed follow-up data on 106 patients of whom 25 had died. The median survival time from the occurrence of first symptoms was 14 years. Mortality risk was significantly higher in patients with an early disease onset. Causes of death were varied, but pneumonia and sudden unexplained deaths were particularly frequent.
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