Implication of the Nutritional and Nonnutritional Factors in the Context of Preservation of Cognitive Performance in Patients With Dementia/Depression and Alzheimer Disease

Aliev, Gjumrakch; Ashraf, Ghulam Md; Kaminsky, Yury G.; Sheikh, Ishfaq Ahmed; Sudakov, S. K.; Yakhno, N. N.; Benberin, Valery V.; Бачурин, С. О.

doi:10.1177/1533317513504614

Cited by 14 publications

(13 citation statements)

References 60 publications

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“…Overall, present multi-modality brain imaging findings indicate that increased LTA and higher MeDi adherence may modulate AD risk through its effects on A β levels and associated neuronal injury in NL adults. These data further support novel treatment strategies aimed at delaying cognitive decline and modifying AD progression through simultaneous implementation of pharmacological and non-pharmacological interventions [ 47 ] [ 48 ]. Candidate non-pharmacological treatments include, but are not limited to, increased sensory input through physical and mental activities, which is directed at improving cerebral blood flow, and nutritional interventions such as diet modification, vitamin supplementation and nutraceuticals [ 48 ].…”

Section: Discussionmentioning

confidence: 62%

Physical Activity, Mediterranean Diet and Biomarkers-Assessed Risk of Alzheimer’s: A Multi-Modality Brain Imaging Study

Matthews¹,

Davies²,

Murray³

et al. 2014

AMI

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Increased physical activity and higher adherence to a Mediterranean-type diet (MeDi) have been independently associated with reduced risk of Alzheimer’s disease (AD). Their association has not been investigated with the use of biomarkers. This study examines whether, among cognitively normal (NL) individuals, those who are less physically active and show lower MeDi adherence have brain biomarker abnormalities consistent with AD.MethodsForty-five NL individuals (age 54 ± 11, 71% women) with complete leisure time physical activity (LTA), dietary information, and cross-sectional 3D T1-weigthed MRI, 11C-Pittsburgh Compound B (PiB) and 18F-fluorodeoxyglucose (FDG) Positron Emission Tomography (PET) scans were examined. Voxel-wise multivariate partial least square (PLS) regression was used to examine the effects of LTA, MeDi and their interaction on brain biomarkers. Age, gender, ethnicity, education, caloric intake, BMI, family history of AD, Apolipoprotein E (APOE) genotype, presence of hypertension and insulin resistance were examined as confounds. Subjects were dichotomized into more and less physically active (LTA+ vs. LTA−; n = 21 vs. 24), and into higher vs. lower MeDi adherence groups (n = 18 vs. 27) using published scoring methods. Spatial patterns of brain biomarkers that represented the optimal association between the images and the groups were generated for all modalities using voxel-wise multivariate Partial Least Squares (PLS) regression.ResultsGroups were comparable for clinical and neuropsychological measures. Independent effects of LTA and MeDi factors were observed in AD-vulnerable brain regions for all modalities (p < 0.001). Increased AD-burden (in particular higher Aβ load and lower glucose metabolism) were observed in LTA− compared to LTA+ subjects, and in MeDi− as compared to MeDi+ subjects. A gradient effect was observed for all modalities so that LTA−/MeDi− subjects had the highest and LTA+/MeDi+ subjects had the lowest AD-burden (p < 0.001), although the LTA × MeDi interaction was significant only for FDG measures (p < 0.03). Adjusting for covariates did not attenuate these relationships.ConclusionLower physical activity and MeDi adherence were associated with increased brain AD-burden among NL individuals, indicating that lifestyle factors may modulate AD risk. Studies with larger samples and longitudinal evaluations are needed to determine the predictive power of the observed associations

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Section: Discussionmentioning

confidence: 62%

Physical Activity, Mediterranean Diet and Biomarkers-Assessed Risk of Alzheimer’s: A Multi-Modality Brain Imaging Study

Matthews¹,

Davies²,

Murray³

et al. 2014

AMI

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“…AD is therefore distinguishing by the accumulation of insoluble Aβ plaques within key regions of the brain. The now famous amyloid cascade hypothesis, which has now dominated this field for many years [13], proposes that brain Aβ generation is the primary influence driving AD pathogenesis. The rest of the disease process, including formation of neurofibrillary tangles containing tau protein, synaptic and neuronal loss, and neuroinflammation is projected to result from an imbalance between Aβ production and its clearance.…”

Section: Introductionmentioning

confidence: 99%

Protein Misfolding and Aggregation in Alzheimer’s Disease and Type 2 Diabetes Mellitus

Ashraf¹,

Greig²,

Khan³

et al. 2014

CNSNDDT

179

103

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In general, proteins can only execute their various biological functions when they are appropriately folded. Their amino acid sequence encodes the relevant information required for correct three-dimensional folding, with or without the assistance of chaperones. The challenge associated with understanding protein folding is currently one of the most important aspects of the biological sciences. Misfolded protein intermediates form large polymers of unwanted aggregates and are involved in the pathogenesis of many human diseases, including Alzheimer’s disease (AD) and Type 2 diabetes mellitus (T2DM). AD is one of the most prevalent neurological disorders and has worldwide impact; whereas T2DM is considered a metabolic disease that detrementally influences numerous organs, afflicts some 8% of the adult population, and shares many risk factors with AD. Research data indicates that there is a widespread conformational change in the proteins involved in AD and T2DM that form β-sheets like motifs. Although conformation of these β-sheets is common to many functional proteins, the transition from α-helix to β-sheet is a typical characteristic of amyloid deposits. Any abnormality in this transition results in protein aggregation and generation of insoluble fibrils. The abnormal and toxic proteins can interact with other native proteins and consequently catalyze their transition into the toxic state. Both AD and T2DM are prevalent in the aged population. AD is characterized by the accumulation of amyloid-β (Aβ) in brain, while T2DM is characterized by the deposition of islet amyloid polypeptide (IAPP, also known as amylin) within beta-cells of the pancreas. T2DM increases pathological angiogenesis and immature vascularisation. This also leads to chronic cerebral hypoperfusion, which results in dysfunction and degeneration of neuroglial cells. With an abundance of common mechanisms underpinning both disorders, a significant question that can be posed is whether T2DM leads to AD in aged individuals and the associations between other protein misfolding diseases.

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“…Healthy diet maintenance is important in the modulation of AD symptoms and pathology, assisting endogenous mechanisms including neurogenesis, antioxidant protection, and Aβ clearance (Aliev et al, 2013 ; Maruszak et al, 2014 ). Type 2 Diabetes Mellitus (T2DM) is an acquired disease caused by hyperglycaemia and potentially insulin resistance.…”

Section: Lifestyle Interventionsmentioning

confidence: 99%

“…Dietary plans have been well researched in AD. The main three are the Mediterranean, ketogenic, and caloric restriction diets (Aliev et al, 2013 ; Maruszak et al, 2014 ). The Mediterranean diet involves replacement of meat products, especially red meat, with plant-based alternatives, and primarily olive and fish oils for additional fats (Yannakoulia et al, 2015 ).…”

Section: Lifestyle Interventionsmentioning

confidence: 99%

Interaction between therapeutic interventions for Alzheimer’s disease and physiological Aβ clearance mechanisms

Morrone

Liu

Black

et al. 2015

Front. Aging Neurosci.

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Most therapeutic agents are designed to target a molecule or pathway without consideration of the mechanisms involved in the physiological turnover or removal of that target. In light of this and in particular for Alzheimer’s disease, a number of therapeutic interventions are presently being developed/investigated which target the amyloid-β peptide (Aβ). However, the literature has not adequately considered which Aβ physiological clearance pathways are necessary and sufficient for the effective action of these therapeutics. In this review, we evaluate the therapeutic strategies targeting Aβ presently in clinical development, discuss the possible interaction of these treatments with pathways that under normal physiological conditions are responsible for the turnover of Aβ and highlight possible caveats. We consider immunization strategies primarily reliant on a peripheral sink mechanism of action, small molecules that are reliant on entry into the CNS and thus degradation pathways within the brain, as well as lifestyle interventions that affect vascular, parenchymal and peripheral degradation pathways. We propose that effective development of Alzheimer’s disease therapeutic strategies targeting Aβ peptide will require consideration of the age- and disease-specific changes to endogenous Aβ clearance mechanisms in order to elicit maximal efficacy.

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Implication of the Nutritional and Nonnutritional Factors in the Context of Preservation of Cognitive Performance in Patients With Dementia/Depression and Alzheimer Disease

Cited by 14 publications

References 60 publications

Physical Activity, Mediterranean Diet and Biomarkers-Assessed Risk of Alzheimer’s: A Multi-Modality Brain Imaging Study

Physical Activity, Mediterranean Diet and Biomarkers-Assessed Risk of Alzheimer’s: A Multi-Modality Brain Imaging Study

Protein Misfolding and Aggregation in Alzheimer’s Disease and Type 2 Diabetes Mellitus

Interaction between therapeutic interventions for Alzheimer’s disease and physiological Aβ clearance mechanisms

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