scholarly journals Metabolic Syndrome, Cognitive Impairment and the Role of Diet: A Narrative Review

Nutrients ◽  
2022 ◽  
Vol 14 (2) ◽  
pp. 333
Author(s):  
Matina Kouvari ◽  
Nathan M. D’Cunha ◽  
Nikolaj Travica ◽  
Domenico Sergi ◽  
Manja Zec ◽  
...  
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Cognitive Impairment ◽  
Cognitive Decline ◽  
Clinical Manifestations ◽  
Narrative Review ◽  
Cognitive Outcomes ◽  
Food Groups ◽  
Cardiometabolic Disorders

Background: This narrative review presents the association between metabolic syndrome (MetS), along with its components, and cognition-related disorders, as well as the potential reversal role of diet against cognitive impairment by modulating MetS. Methods: An electronic research in Medline (Pubmed) and Scopus was conducted. Results: MetS and cognitive decline share common cardiometabolic pathways as MetS components can trigger cognitive impairment. On the other side, the risk factors for both MetS and cognitive impairment can be reduced by optimizing the nutritional intake. Clinical manifestations such as dyslipidemia, hypertension, diabetes and increased central body adiposity are nutrition-related risk factors present during the prodromal period before cognitive impairment. The Mediterranean dietary pattern stands among the most discussed predominantly plant-based diets in relation to cardiometabolic disorders that may prevent dementia, Alzheimer’s disease and other cognition-related disorders. In addition, accumulating evidence suggests that the consumption of specific dietary food groups as a part of the overall diet can improve cognitive outcomes, maybe due to their involvement in cardiometabolic paths. Conclusions: Early MetS detection may be helpful to prevent or delay cognitive decline. Moreover, this review highlights the importance of healthy nutritional habits to reverse such conditions and the urgency of early lifestyle interventions.

The Spectrum of Cerebrovascular Disease and Associated Cognitive Decline

2019 ◽  
pp. 574-599
Author(s):  
Victoria J. Williams ◽  
Steven E. Arnold ◽  
David H. Salat
Keyword(s):  
Risk Factors ◽  
Cognitive Impairment ◽  
Cerebrovascular Disease ◽  
Cognitive Decline ◽  
Vascular Dementia ◽  
Structure And Function ◽  
Vascular Risk Factors ◽  
Vascular Health ◽  
Vascular Risk ◽  
And Function

Throughout the lifespan, common variations in systemic health and illness contribute to alterations in vasculature structure and function throughout the body, significantly increasing risk for cardiovascular and cerebrovascular disease (CVD). CVD is a prevalent cause of mortality in late life; it also promotes brain alterations, contributing to cognitive decline and, when severe, vascular dementia. Even prior to diseased states, individual variation in CVD risk is associated with structural and functional brain alterations. Yet, how cumulative asymptomatic alterations in vessel structure and function contribute to more subtle changes in brain tissue integrity and function that emerge in late life is unclear. Finally, vascular risk factors are associated with the clinical progression of neurodegenerative diseases such as Alzheimer’s disease (AD); however, recent theory posits that vascular degeneration may serve a contributory role in these conditions. This chapter reviews how lifespan changes in vascular health contribute to degenerative changes in neural tissue and the subsequent development of cognitive impairment and/or vascular dementia. It first discusses associations between vascular risk factors and cognition and also how declining vascular health may lead to cognitive impairment and dementia. Next, it identifies basic aspects of cerebrovascular anatomy and physiology sustaining tissue health and discusses how vulnerabilities of this system contribute to neurodegenerative changes. Finally, it reviews evidence of vascular contributions to AD and presents ideas for future research to better understand the full spectrum of cerebrovascular contributions to brain aging, cognitive decline, and dementia.

scholarly journals The Role of High Triglycerides Level in Predicting Cognitive Impairment: A Review of Current Evidence

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 2118
Author(s):  
Alina Mihaela Dimache ◽  
Delia Lidia Șalaru ◽  
Radu Sascău ◽  
Cristian Stătescu
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Decline ◽  
Lifestyle Modification ◽  
Cognitive Disorders ◽  
Current Evidence ◽  
Barrier Dysfunction ◽  
Serum Triglycerides ◽  
Cerebral Amyloidosis ◽  
The Relationship

The burden of cognitive disorders is huge and still growing, however the etiology and the degree of cognitive impairment vary considerably. Neurodegenerative and vascular mechanisms were most frequently assessed in patients with dementia. Recent studies have shown the possible involvement of triglycerides levels in cognitive function through putative mechanisms such as brain blood barrier dysfunction or amyloid metabolism imbalance, but not all research in the field found this association. Several clinical studies evaluated the relationship between different forms of cognitive decline and levels of serum triglycerides, independent of other cardiovascular risk factors. This review focuses on the role of triglycerides in cognitive decline, cerebral amyloidosis and vascular impairment. Considering that the management of hypertriglyceridemia benefits from lifestyle modification, diet, and specific drug therapy, future studies are requested to appraise the triglycerides–cognitive impairment relationship.

Analyses of Visuospatial and Visuoperceptual Errors as Predictors of Dementia in Parkinson’s Disease Patients with Subjective Cognitive Decline and Mild Cognitive Impairment

2020 ◽  
pp. 1-11
Author(s):  
Iván Galtier ◽  
Antonieta Nieto ◽  
María Mata ◽  
Jesús N. Lorenzo ◽  
José Barroso
Keyword(s):  
Risk Factors ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Decline ◽  
Poor Performance ◽  
Subjective Cognitive Decline ◽  
Independent Risk Factors

ABSTRACT Objective: Subjective cognitive decline (SCD) and mild cognitive impairment (MCI) in Parkinson’s disease (PD) are considered as the risk factors for dementia (PDD). Posterior cortically based functions, such as visuospatial and visuoperceptual (VS-VP) processing, have been described as predictors of PDD. However, no investigations have focused on the qualitative analysis of the Judgment of Line Orientation Test (JLOT) and the Facial Recognition Test (FRT) in PD-SCD and PD-MCI. The aim of this work was to study the VS-VP errors in JLOT and FRT. Moreover, these variables are considered as predictors of PDD. Method: Forty-two PD patients and 19 controls were evaluated with a neuropsychological protocol. Patients were classified as PD-SCD and PD-MCI. Analyses of errors were conducted following the procedure described by Ska, Poissant, and Joanette (1990). Follow-up assessment was conducted to a mean of 7.5 years after the baseline. Results: PD-MCI patients showed a poor performance in JLOT and FRT total score and made a greater proportion of severe intraquadrant (QO2) and interquadrant errors (IQO). PD-SCD showed a poor performance in FRT and made mild errors in JLOT. PD-MCI and QO2/IQO errors were independent risk factors for PDD during the follow-up. Moreover, the combination of both PD-MCI diagnosis and QO2/IQO errors was associated with a greater risk. Conclusions: PD-MCI patients presented a greater alteration in VS-VP processing observable by the presence of severe misjudgments. PD-SCD patients also showed mild difficulties in VS-SP functions. Finally, QO2/IQO errors in PD-MCI are a useful predictor of PDD, more than PD-MCI diagnosis alone.

scholarly journals Risk of progression from subjective cognitive decline to mild cognitive impairment: The role of study setting

2018 ◽  
Vol 14 (6) ◽  
pp. 734-742 ◽  
Author(s):  
Beth E. Snitz ◽  
Tianxiu Wang ◽  
Yona Keich Cloonan ◽  
Erin Jacobsen ◽  
Chung-Chou H. Chang ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Decline ◽  
Subjective Cognitive Decline ◽  
Risk Of Progression ◽  
Study Setting

The role of Mediterranean diet in the course of subjective cognitive decline in the elderly population of Greece: results from a prospective cohort study

2021 ◽  
pp. 1-29
Author(s):  
George S. Vlachos ◽  
Mary Yannakoulia ◽  
Costas A. Anastasiou ◽  
Mary H. Kosmidis ◽  
Efthimios Dardiotis ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Mediterranean Diet ◽  
The Elderly ◽  
Protective Role ◽  
Subjective Cognitive Decline ◽  
Preventive Strategy ◽  
Food Groups ◽  
Medical Disorders ◽  
The Mediterranean

Abstract Very few data are available regarding the association of adherence to the Mediterranean Diet (MeDi) with Subjective Cognitive Decline (SCD) evolution over time. A cohort of 939 cognitively normal individuals reporting self-experienced, persistent cognitive decline not attributed to neurological, psychiatric or medical disorders from the Hellenic Epidemiological Longitudinal Investigation of Aging and Diet (HELIAD study) was followed-up for a mean period of 3.10 years. We defined our SCD score as the number of reported SCD domains (memory, language, visuoperceptual and executive), ranging from 0 to 4. Dietary intake at baseline was assessed through a food frequency questionnaire; adherence to the MeDi pattern was evaluated through the Mediterranean Diet Score (MDS) that ranged from 0 to 55, with higher values indicating greater adherence to the MeDi. The mean SCD score in our cohort increased by 0.20 cognitive domains during follow-up. After adjustment for multiple potential confounders, we showed that an MDS higher by 10 points was associated with a 7% reduction in the progression of SCD within one year. In terms of food groups, every additional vegetable serving consumption per day was associated with a 2.3% reduction in SCD progression per year. Our results provide support to the notion that MeDi may have a protective role against the whole continuum of cognitive decline, starting at the first subjective complaints. This finding may strengthen the role of the MeDi as a population-wide, cost-effective preventive strategy targeting the modifiable risk factors for cognitive decline.

The role of high-mobility group box protein 1 in chronic cerebral hypoperfusion-induced vascular cognitive impairment animals

2019 ◽  
Author(s):  
Amelia Nur Vidyanti ◽  
Jia-Yu Hsieh ◽  
Kun-Ju Lin ◽  
Yao-Ching Fang ◽  
Ismail Setyopranoto ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Decline ◽  
High Mobility ◽  
Vascular Cognitive Impairment ◽  
High Mobility Group ◽  
Cerebral Hypoperfusion ◽  
Hippocampal Atrophy ◽  
Amyloid Pet ◽  
Knock Out

Abstract Background: The molecular mechanisms of vascular cognitive impairment (VCI) are diverse and still in puzzle. VCI could be attributed to chronic cerebral hypoperfusion (CCH). CCH may cause a cascade of reactions involved in ischemia and neuro-inflammation which plays important roles in the pathophysiology of VCI. High-mobility group box protein 1 (HMGB1) is a non-histone protein that serves as a damage-associated molecular signal leading to cascades of inflammation. Increased level of HMGB1 has been established in the acute phase of CCH. However, the role of HMGB1 at the chronic phase of CCH remains elucidated. Methods: We performed modified bilateral common carotid artery occlusion (BCCAO) in C57BL/6 mice to induce CCH. We examined the cerebral blood flow (CBF) reduction by laser doppler flowmetry, the protein expression of HMGB1 and its pro-inflammatory cytokines (TNF-a, IL-1b, and IL-6) by western blotting and immunohistochemistry. The brain pathology was assessed by 7T-animal MRI and amyloid-b accumulation was assessed by amyloid-PET scanning. We further evaluated the effect of HMGB1 suppression by injecting CRISPR/Cas9 knock-out plasmid intra-hippocampus bilaterally. Results: There were reduction of CBF up to 50% which persisted three months after CCH. The modified-BCCAO animals developed significant cognitive decline. The 7T-MRI image showed hippocampal atrophy, although the amyloid-PET showed no significant amyloid-beta accumulation. Increased protein levels of HMGB1, TNF-a and IL-1b were found three months after BCCAO. HMGB1 suppression by CRISPR/Cas9 knock-out plasmid restored the CBF, IL-1B, TNF-alpha, IL-6, and attenuated hippocampal atrophy and cognitive decline. Conclusion: HMGB1 plays a pivotal role in the pathophysiology of the animal model of CCH and it might be a candidate as therapeutic targets of VCI.

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