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Protein intake for cognitive function

Protein intake for cognitive function

Cognitive functions were assessed Funnction a series of cognitive tests. FAO Food and Nutrition Paper No. Relative intake of macronutrients impacts risk of mild cognitive impairment or dementia. Protein intake for cognitive function

Protein intake for cognitive function -

We observed a consistent upregulation of cytokines CXCL10 , CCL3 following immune challenge across cell types, including microglia. Such in vitro patterns of expression following an immune challenge indicate the positive associations of inflammatory diet with candidate proteins in the current study may reflect pro-inflammatory responses CXCL10, CCL3 or compensatory, anti-inflammatory patterns of regulation NFATC3, HGF, CDCP1 that alter risk for subsequent cognitive impairment.

To further understand candidate protein biology and determine their potential role in AD, we utilized several complementary, publicly available resources. Using STRING protein-protein interaction network analyses and functional enrichment, we found that three of our candidate proteins CXCL10, CCL3, HGF involved in cellular locomotion in response to chemical stimulus i.

Leveraging data obtained from comprehensive post-mortem brain tissue collections, along with expression data via the AMP-AD Sage Bionetworks Agora platform, we also observed five of our candidate proteins OPG, HGF, NFATC3, CDCP1, ITGA11 display upregulated expression in the brains of AD individuals and maintain expression quantitative trait loci eQTL in brain tissue.

These results suggest that at least five of the seven inflammatory diet proteins identified in plasma and linked to cognitive impairment may be differentially expressed in the brains of individuals at risk for AD and regulated, at least in part, by underlying genetic variation Fig.

While one of the proteins linked to EDII and incident cognitive impairment CXCL10 has been nominated as a therapeutic target for AD, three candidate proteins CCL2, CXCL10, and HGF are therapeutic targets of ongoing clinical trials for non-neurologic disease Supplementary Table The current findings provide insights into how inflammatory nutritional patterns relate to an immune-related plasma proteome.

Together, these results highlight the molecular mediators through which an inflammatory diet may contribute to the risk for age-related cognitive impairment and dementia. While previous investigations have demonstrated a relationship between inflammatory diet and a select group of inflammatory proteins e.

Several lines of evidence indicate that the patterns of protein expression reported here indeed reflect diets with differing inflammatory potential. First, we observed significant correlations of EDII scores with increasing levels of IL-6 and TNF, two pro-inflammatory cytokines previously used to validate anti-inflammatory diets e.

In addition, many of the proteins significantly correlated with energy-adjusted diet scores in our study FGF, IL-6, ILR1, FGF, CSF-1, HGF, CCL20, ILB, VEGFA, ILRB, IL, TRANCE, CCL3, CDCP1, TWEAK were also related to BMI in a recently published RCT, where changes in these proteins also tracked changes in BMI following a healthy dietary intervention [ 33 ].

The upregulation of nine immunologically relevant pathways in the context of higher EDII scores further supports the concept of a broad, diet-induced immune stimulation, and calls attention to specific cellular processes extracellular matrix organization, inflammatory response, response to cytokine stimulus by which pro-inflammatory diets may contribute to disrupted cellular homeostasis.

Notably, the apoptotic process composite score, which was positively associated with baseline EDII scores as well as incident cognitive impairment in this study, was also found in the Swedish BioFINDER study to distinguish amyloid-positive AD and amyloid-positive MCI participants from amyloid-negative cognitively normal and MCI individuals [ 35 ].

Adding to these previous findings, our results suggest that the regulation of proteins in this cell-death signaling cascade may be augmented by an inflammatory diet and relate—perhaps mechanistically—to amyloid deposition, at least during the initial stages of cognitive decline. The candidate proteins we identified have been associated with cognitive decline in other studies using similar proteomic assays, providing further support to our findings.

Higher plasma levels of CDCP1, OPG, and HGF have been shown to accurately discriminate dementia cases from cognitively normal older adults [ 58 , 59 , 60 ]. Furthermore, differing concentrations of plasma ITGA11 and NFATC3, and elevated intrathecal CCL3 have been observed among individuals diagnosed with AD, while abnormal levels of CXCL10 in CSF or plasma are found across multiple neurodegenerative phenotypes, including FTD and AD [ 59 , 61 , 62 , 63 ].

Of note, we observed consistency in directionality of the relationship between protein level and cognitive impairment, i. The consistency of these results reinforces prior studies that report increased dementia incidence tied to pro-inflammatory diets [ 11 , 12 , 13 , 14 , 15 ] and extends these findings by revealing specific plasma proteins that may link an inflammatory diet to cognitive dysfunction in aging.

Our assessment of inflammatory diet proteins in relation to plasma biomarkers of AD pathology and neurodegeneration adds to the limited understanding of how dietary patterns may influence pathological processes within the CNS [ 64 , 65 , 66 ]. Of the seven plasma proteins linked to pro-inflammatory diet and cognitive impairment, four and three were positively associated with NfL and an MRI measure of AD-relevant brain atrophy, respectively.

These findings support the well-documented relationship between peripheral inflammation and neurodegeneration [ 67 , 68 , 69 , 70 ]. These results are consistent with recent data suggesting immune activation may limit deposition of brain Aβ among individuals at-risk for cognitive deficits [ 71 , 72 , 73 ].

While it is unlikely that an inflammatory diet has a protective effect on Aβ pathology, individuals predisposed to mount a more robust immune response to an inflammatory diet may also mount a stronger response to brain Aβ deposition, at least initially.

While the observational nature of this study precludes any determination of causality, our results nonetheless suggest that proteins linked to an inflammatory diet may contribute to neuronal injury.

We note, however, that although we show CCL3 and OPG are positively associated with neurodegeneration biomarkers in two separate cohorts, other investigations have failed to find associations between plasma CCL3, OPG, and atrophy in brain regions commonly implicated in AD [ 74 , 75 ].

These three proteins may be especially responsive to immunologic stressors, and in the context of our results, may play a role in regulating the effects of pro-inflammatory processes on target cells within the brain. While all five proteins have been previously implicated in AD, our results suggest that an inflammatory diet may be a key driver of these AD-associated proteins [ 58 , 59 , 60 , 61 , 62 , 63 ].

Interestingly, three of the seven candidate proteins are cytokines with known patterns of co-expression. One of these proteins, CXCL10 also known as interferon gamma-induced protein 10 , acts as a ligand for CXCR3, thereby promoting activation of monocytes and natural killer cells, as well as the migration of T-cells [ 76 ].

Accordingly, CXCL10 has been nominated by the Accelerated Medicine Partnership as a potential therapeutic target for AD.

First, because of the goals of the parent study WHIMS ancillary study , participants were limited to white women. Although protein-dementia associations replicated in more diverse external samples, additional studies will be needed to determine the generalizability of results to other demographic groups.

Second, the use of a matched case-control design for the WHIMS ancillary study precluded the use of time-to-event analyses, which may be better suited to detect protein-cognitive impairment associations. Third, while an inflammatory diet was previously associated with risk for incident cognitive impairment in a group of participants from the parent WHIMS study [ 14 ], the current analysis was restricted to a more deeply phenotyped subset of participants at approximately one-fifth the size.

In turn, limited power to detect the DII-cognitive impairment association demonstrated previously precluded the use of formal mediation models. Fourth, given the observational nature of this study, the extent to which diet and proteins exert causal effects, as well as the directionality of these effects, are unknown.

We encourage future preclinical investigations to establish temporal precedence and the associated causality between components of pro-inflammatory diets e. Fifth, the associations between inflammatory protein levels and inflammatory diet scores were weak, consistent with prior reports [ 29 , 78 , 79 , 80 ].

or that measurement error inherent in the retrospective self-reported dietary assessment [ 81 ] attenuated true associations between inflammatory diet scores and inflammatory protein levels. Additionally, biological fluctuations e. Therefore, null effects should be interpreted with appropriate caution.

However, numerous studies have demonstrated that outside the context of an acute infection or injury, levels for many inflammatory proteins—and plasma proteins more broadly—remain relatively stable across time [ 83 , 84 ]. Despite these limitations, the current results provide insights into the molecular conduits through which pro-inflammatory nutritional habits may contribute to cognitive impairment.

Follow-up studies will be needed to determine whether the identified proteins indeed play a causal, mechanistic role in late-life cognitive decline and dementia.

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The WHI program is funded by the National Heart, Lung, and Blood Institute, National Institutes of Health, U. Department of Health and Human Services through contracts 75ND, 75ND, 75ND, 75ND, 75ND Similar to WHI, The Atherosclerosis Risk in Communities Study ARIC is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts 75ND, 75ND, 75ND, 75ND, 75ND The ARIC Neurocognitive Study is additionally supported by U01HL, U01HL, U01HL, U01HL, and U01HL from the NIH NHLBI, NINDS, NIA, and NIDCD.

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Download references. We thank all individuals at the National Center for Health Statistics of the Centers for Disease Control and Prevention who were responsible for the planning and administering of NHANES and making the datasets of NHANES available on their website.

Department of Epidemiology and Health Statistics, Public Health College, Qingdao University, Qingdao, Shandong, China. You can also search for this author in PubMed Google Scholar.

Objectives: The cognltive of this ontake Protein intake for cognitive function to rPotein the association of dietary Magnesium for athletic performance intake and protein sources with cognitive function ontake population aged 60 years and older. Design: Cross-sectional study. Setting: The National Health and Nutrition Examination Survey NHANES Participants: Non-institutionalized US adults aged 60 years and older. Measurements: Cognitive functions were assessed by a series of cognitive tests. Dietary protein intake was assessed by two hour dietary recall interviews. Background: To delay the onset of dementia, it is important Energizing thirst quenchers healthy adults to take Protein intake for cognitive function actions before the intke function clearly declines. Coognitive purpose of this study was to Nutrition for team sports the effect of the ingestion fynction seven selected cogitive Protein intake for cognitive function acids as a granular powder, namely, leucine, phenylalanine, and lysine supplemented with isoleucine, histidine, valine, and tryptophan on cognitive and psychosocial functions in healthy adults. Methods: A double-blind, randomized, placebo-controlled trial was conducted. A total of participants aged 55 years or older were randomly assigned to one of three groups: daily ingestion of 3 g 3gIG or 6 g 6gIG of the selected amino acids or daily ingestion of a placebo PCG. Each group ingested the test powder for 12 weeks.


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