scholarly journals Neuroinflammation and functional connectivity in Alzheimer’s disease: interactive influences on cognitive performance

2019 ◽  
Author(s):  
L. Passamonti ◽  
K.A. Tsvetanov ◽  
P.S. Jones ◽  
W.R. Bevan-Jones ◽  
R. Arnold ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Functional Connectivity ◽  
Cognitive Deficits ◽  
Large Scale ◽  
Temporal Cortex ◽  
Network Connectivity ◽  
Cognitive Status ◽  
Network Function

AbstractNeuroinflammation is a key part of the etio-pathogenesis of Alzheimer’s disease. We test the relationship between neuroinflammation and the disruption of functional connectivity in large-scale networks, and their joint influence on cognitive impairment.We combined [11C]PK11195 positron emission tomography (PET) and resting-state functional magnetic resonance imaging (rs-fMRI) in 28 humans (13 females/15 males) with clinical diagnosis of probable Alzheimer’s disease or mild cognitive impairment with positive PET biomarker for amyloid, and 14 age-, sex-, and education-matched healthy humans (8 females/6 males). Source-based ‘inflammetry’ was used to extract principal components of [11C]PK11195 PET signal variance across all participants. rs-fMRI data were pre-processed via independent component analyses to classify neuronal and non-neuronal signals. Multiple linear regression models identified sources of signal co-variance between neuroinflammation and brain connectivity profiles, in relation to group and cognitive status.Patients showed significantly higher [11C]PK11195 binding relative to controls, in a distributed spatial pattern including the hippocampus, medial, and inferior temporal cortex. Patients with enhanced loading on this [11C]PK11195 binding distribution displayed diffuse abnormal functional connectivity. The expression of a stronger association between such abnormal connectivity and higher levels of neuroinflammation correlated with worse cognitive deficits.Our study suggests that neuroinflammation relates to the pathophysiological changes in network function that underlie cognitive deficits in Alzheimer’s disease. Neuroinflammation, and its association with functionally-relevant reorganisation of brain networks, is proposed as a target for emerging immuno-therapeutic strategies aimed at preventing or slowing the emergence of dementia.Significance StatementNeuroinflammation is an important aspect of Alzheimer’s disease (AD), but it was not known whether the influence of neuroinflammation on brain network function in humans was important for cognitive deficit.Our study provides clear evidence that in vivo neuroinflammation in AD impairs large-scale network connectivity; and that the link between inflammation and functional network connectivity is relevant to cognitive impairment.We suggest that future studies should address how neuroinflammation relates to network function as AD progresses; and whether the neuroinflammation in AD is reversible, as the basis of immunotherapeutic strategies to slow the progression of AD.

scholarly journals Effects of Anosognosia on Perceived Stress and Cortisol Levels in Alzheimer’s Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Genevieve Arsenault-Lapierre ◽  
Victor Whitehead ◽  
Sonia Lupien ◽  
Howard Chertkow
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Perceived Stress ◽  
Cognitive Deficits ◽  
Salivary Cortisol ◽  
Newly Diagnosed ◽  
Stress Scale ◽  
Cortisol Levels

Anosognosia, or unawareness of one’s own cognitive deficits, may cause issues when measuring perceived stress and cortisol levels in Alzheimer’s disease (AD) and Mild Cognitive Impairment (MCI). The goal of this study was to examine the effects of anosognosia on perceived stress and salivary cortisol levels in normal elderly (NE) adults, MCI individuals, newly diagnosed AD patients, and long-lasting AD patients, suspected to show more anosognosia. An anosognosia index for perceived stress was computed by subtracting the score on the Perceived Stress Scale measured in the participants and their relative. Cortisol levels were measured four times a day over two nonconsecutive days. Greater anosognosia for dementia correlated with greater anosognosia for perceived stress in the group as a whole. However, no correlation between cortisol levels and either anosognosia for dementia or perceived stress was observed. Our results suggest that measuring perceived stress in AD patients may be influenced by anosognosia.

Diagnostic utility of sound naming in early Alzheimer’s disease

2009 ◽  
Vol 15 (2) ◽  
pp. 231-238 ◽  
Author(s):  
HYEON-AE JEON ◽  
KYOUNG-MIN LEE
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Picture Naming ◽  
Temporal Cortex ◽  
Cognitive Domain ◽  
Diagnostic Utility ◽  
Future Studies ◽  
Early Alzheimer’S Disease

AbstractWhile it is well known that picture naming (PN) is impaired in Alzheimer’s disease (AD), sound naming (SN) has not been thoroughly investigated. We postulated that SN might be impaired more severely and earlier than PN, given the early involvement of the temporal cortex by AD-related pathology. SN and PN were assessed in 21 normal participants, 40 patients with mild cognitive impairment (MCI), and 27 patients in early stages of AD. Our results showed that SN accuracy and latency were more sensitive to advancing pathology in AD than PN accuracy and latency. SN was more useful and specific in distinguishing MCI patients from normal participants and therefore in potentially identifying the subset of MCI patients who already have impairment in more than one cognitive domain and may actually have incipient AD. These findings indicate a potential diagnostic utility of SN for early detection of the disease. Furthermore, even though most AD patients demonstrated more or less comparable impairment in both tasks, some were disproportionately impaired on SN and others were differentially impaired on PN. Future studies may be able to show that these discrepant groups correspond to patients with right and left hemisphere predominant AD, respectively. (JINS, 2009, 15, 231–238.)

scholarly journals Nutrition and cognitive impairment in the elderly

2001 ◽  
Vol 86 (3) ◽  
pp. 313-321 ◽  
Author(s):  
M. González-Gross ◽  
Ascensión Marcos ◽  
Klaus Pietrzik
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Large Scale ◽  
Public Health Problem ◽  
The Elderly ◽  
Vitamin B ◽  
Clinical Onset ◽  
Related Risk

As the number of older people is growing rapidly worldwide and the fact that elderly people are also apparently living longer, dementia, the most common cause of cognitive impairment is getting to be a greater public health problem. Nutrition plays a role in the ageing process, but there is still a lack of knowledge about nutrition-related risk factors in cognitive impairment. Research in this area has been intensive during the last decade, and results indicate that subclinical deficiency in essential nutrients (antioxidants such as vitamins C, E and β-carotene, vitamin B12, vitamin B6, folate) and nutrition-related disorders, as hypercholesterolaemia, hypertriacylglycerolaemia, hypertension, and diabetes could be some of the nutrition-related risk factors, which can be present for a long time before cognitive impairment becomes evident. Large-scale clinical trials in high-risk populations are needed to determine whether lowering blood homocysteine levels reduces the risk of cognitive impairment and may delay the clinical onset of dementia and perhaps of Alzheimer's disease. A curative treatment of cognitive impairment, especially Alzheimer's disease, is currently impossible. Actual drug therapy, if started early enough, may slow down the progression of the disease. Longitudinal studies are required in order to establish the possible link of nutrient intake – nutritional status with cognitive impairment, and if it is possible, in fact, to inhibit or delay the onset of dementia.

scholarly journals Resting-State Connectivity of Auditory and Reward Systems in Alzheimer’s Disease and Mild Cognitive Impairment

2020 ◽  
Author(s):  
Diana Wang ◽  
Alexander Belden ◽  
Suzanne Hanser ◽  
Maiya R. Geddes ◽  
Psyche Loui
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Functional Connectivity ◽  
Resting State ◽  
Healthy Aging ◽  
Superior Temporal Gyrus ◽  
Healthy Controls ◽  
Reward Systems

AbstractMusic-based interventions have become increasingly widely adopted for dementia and related disorders. Previous research shows that music engages reward-related regions through functional connectivity with the auditory system. Here we characterize intrinsic connectivity of the auditory and reward systems in healthy aging, mild cognitive impairment (MCI) - a predementia phase of cognitive dysfunction, and Alzheimer’s disease (AD). Using resting-state fMRI data from the Alzheimer’s Database Neuroimaging Initiative, we tested functional connectivity within and between auditory and reward systems in older adults with MCI, AD, and age-matched healthy controls (N=105). Seed-based correlations were assessed from regions of interest (ROIs) in the auditory network, i.e. anterior superior temporal gyrus (aSTG), posterior superior temporal gyrus (pSTG), Heschl’s Gyrus, and reward network (i.e., nucleus accumbens, caudate, putamen, and orbitofrontal cortex [OFC]). AD individuals were lower in both within-network and between-network functional connectivity in the auditory network and reward networks compared to MCI and healthy controls. Furthermore, graph theory analyses showed that MCI individuals had higher clustering, local efficiency, degrees, and strengths than both AD individuals and healthy controls. Together, the auditory and reward systems show preserved within- and between-network connectivity in MCI relative to AD. These results suggest that music-based interventions have the potential to make an early difference in individuals with MCI, due to the preservation of functional connectivity in reward-related regions and between auditory and reward networks at that initial stage of neurodegeneration.

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