Blood-based biomarkers in hypothalamic-pituitary axes for the risk of dementia or cognitive decline: a systematic review and meta-analysis.
Ontology highlight
ABSTRACT:
SUBMITTER: Ge YJ
PROVIDER: S-EPMC7655197 | biostudies-literature | 2020 Oct
REPOSITORIES: biostudies-literature
Publications
Blood-based biomarkers in hypothalamic-pituitary axes for the risk of dementia or cognitive decline: a systematic review and meta-analysis.
Ge Yi-Jun YJ Xu Wei W Tan Chen-Chen CC Tan Lan L
Aging 20201026 20
Blood-based biomarkers are ideal candidates for dementia prediction. This systematic review and meta-analysis aimed to evaluate longitudinal relationships of blood hormones and hormone-binding proteins in hypothalamic-pituitary (HP) axes with dementia or cognitive decline. PubMed, MEDLINE, EMBASE, PsycINFO, and BIOSIS were systematically searched from 1919 to June 2020. Fifteen types of hormones and four types of hormone-binding proteins were measured in 48 prospective studies. Increased risk of ...[more]
Similar Datasets
Project description:Objective:Neuroendocrine dysfunction is related to the pathogenesis of mental disorders, but conclusions from clinical research lack consistency. We aimed to investigate the neuroendocrinal pathophysiology and its correlation with clinical symptoms in patients with schizophrenia. Methods:The present cross-sectional study included 486 inpatients with schizophrenia admitted at a psychiatric hospital in Shanghai within one year, and 154 healthy controls (HC) matched on age and gender. The serum hemoconcentrations of thyroid-stimulating hormone (TSH), total triiodothyronine (TT3), total thyroxine (TT4), free triiodothyronine (FT3), free thyroxine (FT4), adrenocorticotrophic hormone (ACTH), and cortisol (COR) were measured via electrochemical luminescence immunoassay. Pathophysiological conversions of neuroendocrine were then associated with gender, age, age at onset, antipsychotic treatment using hierarchical multiple linear regression. Results:When compared to HC, the schizophrenia group showed elevated ACTH and COR levels and decreased TT3 and TT4 levels (p's < 0.05). First-episode patients showed lower TSH and higher FT3 and FT4 (p's < 0.05) compared to recurrent patients. Female patients showed higher TSH and lower TT3, FT3, and ACTH levels (p's < 0.05) compared to males. We observed the area under the curve (AUC) of the predictive model to distinguish between schizophrenia and HC to be 0.737 among total samples and between first-episode and recurrent schizophrenia to be 0.890 among subgroups. Conclusions:Decreased TT3 and TT4 and elevated ACTH and COR levels appear to be associated with schizophrenia symptoms. The chronic recurrent trait of schizophrenia may cause long-term effects on FT3 and FT4 while changes in thyroid, and adrenal function as a result of mental disorder varied with gender. The pathophysiological parameters provide fair to good accuracy of these models.
| S-EPMC7056840 | biostudies-literature
Project description:There are no blood-based biomarkers for cognitive decline in aging, or mild cognitive impairment (MCI) and Alzheimer's disease (AD). Cumulative evidence suggests that apolipoproteins, complement system, and transthyretin are involved in AD pathogenesis by sequestration of amyloid ?. However, there is no clinical study to assess the utility of "sequester proteins" in risk assessment and/or diagnosis of MCI and AD.Serum levels of sequester proteins and their clinical potential in cognitive decline assessment were analyzed by longitudinal and cross-sectional studies using independent cohorts and were confirmed by a prospective study.A combination of apolipoprotein A1, complement C3, and transthyretin achieved an area under the curve of 0.89 (sensitivity 91% and specificity 80%) in MCI versus healthy controls and also discriminated individuals with mild cognitive decline from healthy controls.A set of sequester proteins could be blood-based biomarkers for assessment of early stages of cognitive decline.
| S-EPMC4876892 | biostudies-other
Project description:BACKGROUND: Nicotine may aid reaction time, learning and memory, but smoking increases cardiovascular risk. Cardiovascular risk factors have been linked to increased risk of dementia. A previous meta-analysis found that current smokers were at higher risk of subsequent dementia, Alzheimer's disease, vascular dementia and cognitive decline. METHODS: In order to update and examine this further a systematic review and meta-analysis was carried out using different search and inclusion criteria, database selection and more recent publications. Both reviews were restricted to those aged 65 and over. RESULTS: The review reported here found a significantly increased risk of Alzheimer's disease with current smoking and a likely but not significantly increased risk of vascular dementia, dementia unspecified and cognitive decline. Neither review found clear relationships with former smoking. CONCLUSION: Current smoking increases risk of Alzheimer's disease and may increase risk of other dementias. This reinforces need for smoking cessation, particularly aged 65 and over. Nicotine alone needs further investigation.
| S-EPMC2642819 | biostudies-other
Project description:ImportanceOptimal blood pressure (BP) targets for the prevention of cognitive impairment remain uncertain.ObjectiveTo explore the association of intensive (ie, lower than usual) BP reduction vs standard BP management with the incidence of cognitive decline and dementia in adults with hypertension.Data sources and study selectionA systematic review and meta-analysis of randomized clinical trials that evaluated the association of intensive systolic BP lowering on cognitive outcomes by searching MEDLINE, Embase, CENTRAL, Web of Science, CINAHL, PsycINFO, the International Clinical Trials Registry Platform, and ClinicalTrials.gov from database inception to October 27, 2020.Data extraction and synthesisData screening and extraction were performed independently by 2 reviewers based on Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines. The risk of bias was assessed using the Cochrane risk of bias 2 tool. Random-effects models with the inverse variance method were used for pooled analyses. The presence of potential heterogeneity was evaluated with the I2 index.Main outcomes and measuresThe primary outcome was cognitive decline. Secondary outcomes included the incidence of dementia, mild cognitive impairment (MCI), cerebrovascular events, serious adverse events, and all-cause mortality.ResultsFrom 7755 citations, we identified 16 publications from 5 trials with 17 396 participants (mean age, 65.7 years [range, 63.0-80.5 years]; 10 562 [60.5%] men) and 2 additional ongoing trials. All 5 concluded trials included in quantitative analyses were considered at unclear to high risk of bias. The mean follow-up duration was 3.3 years (range, 2.0 to 4.7 years). Intensive BP reduction was not significantly associated with global cognitive performance (standardized mean difference, 0.01; 95% CI, -0.04 to 0.06; I2 = 0%; 4 trials; 5246 patients), incidence of dementia (risk ratio [RR], 1.09; 95% CI, 0.32 to 3.67; I2 = 27%; 2 trials; 9444 patients) or incidence of MCI (RR, 0.91; 95% CI, 0.73 to 1.14; I2 = 74%; 2 trials; 10 774 patients) when compared with standard treatment. However, a reduction of cerebrovascular events in the intensive group was found (RR, 0.79; 95% CI, 0.67 to 0.93; I2 = 0%; 5 trials; 17 396 patients) without an increased risk of serious adverse events or mortality.Conclusions and relevanceIn this study, there was no significant association between BP reduction and lower risk of cognitive decline, dementia, or MCI. The certainty of this evidence was rated low because of the limited sample size, the risk of bias of included trials, and the observed statistical heterogeneity. Therefore, current available evidence does not justify the use of lower BP targets for the prevention of cognitive decline and dementia.
| S-EPMC8609411 | biostudies-literature
Project description:Background: More people with cognitive dysfunction and dementia also fall into the category of high vascular risk, for which aspirin is one of the most frequently used drugs. However, previous studies reporting that aspirin buffers against mild cognitive decline (MCI) and dementia remain controversial. We thus conducted an updated systematic review and meta-analysis to evaluate the association of aspirin use with the risk of MCI and dementia in older adults. Methods: Data sources from PubMed, Embase, Web of Science, and the Cochrane Database for randomized controlled trails (RCTs) and cohort studies (published between January 1, 2000 and April 11, 2020). Relative risks (RRs) and 95% confidence intervals (95% CIs) were used to pool data on the occurrence of dementia and MCI with random-effects models. Results: Of 3,193 identified articles, 15 studies (12 cohort studies and three RCTs) were eligible and were included in our analysis, which involved a total of 100,909 participants without cognitive dysfunctions or dementia at baseline. In pooled cohort studies, aspirin use did not reduce the incidence of MCI and dementia (the pooled RR = 0.97; 95% CI = 0.85-1.11; Ifor heterogeneity2 = 65%) compared with non-users. However, low-dose aspirin (75-100 mg/day) was associated with a decreased likelihood of developing dementia or MCI (the pooled RR = 0.75; 95% CI = 0.63-0.9; Ifor heterogeneity2 = 50.5%). This association existed in studies including all-cause dementia (the pooled RR = 0.82; 95% CI = 0.71-0.96) and Alzheimer's disease (AD) (the pooled RR = 0.54; 95% CI = 0.33-0.89), but not in MCI (the pooled RR = 0.58; 95% CI = 0.31-1.08). In RCTs, low-dose aspirin use was not significantly associated with less prevalence of dementia or MCI (RR = 0.94; 95% CI = 0.84-1.05; Ifor heterogeneity2 = 0.0%). Conclusions: In cohort studies, we found that low-dose aspirin use had a higher likelihood of reducing the incidence of dementia, which was not supported by RCTs. The evidence was insufficient to fully evaluate the effect of aspirin on cognitive function and dementia. Well-designed studies and innovative approaches are therefore needed to clarify whether the use of aspirin improves cognitive function and reduces the risk of dementia.
| S-EPMC7890199 | biostudies-literature
Project description:BackgroundEmerging evidence indicates that poor periodontal health adversely impacts cognition. This review examined the available longitudinal evidence concerning the effect of poor periodontal health on cognitive decline and dementia.MethodsComprehensive literature search was conducted on five electronic databases for relevant studies published until April 2022. Longitudinal studies having periodontal health as exposure and cognitive decline and/or dementia as outcomes were considered. Random effects pooled estimates and 95% confidence intervals were generated (pooled odds ratio for cognitive decline and hazards ratio for dementia) to assess whether poor periodontal health increases the risk of cognitive decline and dementia. Heterogeneity between studies was estimated by I2 and the quality of available evidence was assessed through quality assessment criteria.ResultsAdopted search strategy produced 2132 studies for cognitive decline and 2023 for dementia, from which 47 studies (24 for cognitive decline and 23 for dementia) were included in this review. Poor periodontal health (reflected by having periodontitis, tooth loss, deep periodontal pockets, or alveolar bone loss) was associated with both cognitive decline (OR = 1.23; 1.05-1.44) and dementia (HR = 1.21; 1.07-1.38). Further analysis, based on measures of periodontal assessment, found tooth loss to independently increase the risk of both cognitive decline (OR = 1.23; 1.09-1.39) and dementia (HR = 1.13; 1.04-1.23). Stratified analysis based on the extent of tooth loss indicated partial tooth loss to be important for cognitive decline (OR = 1.50; 1.02-2.23) and complete tooth loss for dementia (HR = 1.23; 1.05-1.45). However, the overall quality of evidence was low, and associations were at least partly due to reverse causality.ConclusionsPoor periodontal health and tooth loss appear to increase the risk of both cognitive decline and dementia. However, the available evidence is limited (e.g., highly heterogenous, lacking robust methodology) to draw firm conclusions. Further well-designed studies involving standardized periodontal and cognitive health assessment and addressing reverse causality are highly warranted.
| S-EPMC9826143 | biostudies-literature
Project description:IntroductionEvidence from epidemiology, neuroimaging, and animal models indicates that asthma adversely affects the brain, but the nature and extent of neuropathophysiological impact remain unclear.MethodsWe tested the hypothesis that asthma is a risk factor for dementia by comparing cognitive performance and cerebrospinal fluid biomarkers of glial activation/neuroinflammation, neurodegeneration, and Alzheimer's disease (AD) pathology in 60 participants with asthma to 315 non-asthma age-matched control participants (45-93 years), in a sample enriched for AD risk.ResultsParticipants with severe asthma had higher neurogranin concentrations compared to controls and those with mild asthma. Positive relationships between cardiovascular risk and concentrations of neurogranin and α-synuclein were amplified in severe asthma. Severe asthma also amplified the deleterious associations that apolipoprotein E ε4 carrier status, cardiovascular risk, and phosphorylated tau181/amyloid beta42 have with rate of cognitive decline.DiscussionOur data suggest that severe asthma is associated with synaptic degeneration and may compound risk for dementia posed by cardiovascular disease and genetic predisposition.HighlightsThose with severe asthma showed evidence of higher dementia risk than controls evidenced by: higher levels of the synaptic degeneration biomarker neurogranin regardless of cognitive status, cardiovascular or genetic risk, and controlling for demographics.steeper increase in levels of synaptic degeneration biomarkers neurogranin and α-synuclein with increasing cardiovascular risk.accelerated cognitive decline with higher cardiovascular risk, genetic predisposition, or pathological tau.
| S-EPMC9270636 | biostudies-literature
Project description:Preclinical prediction of Alzheimer disease (AD) is important and critical to effective intervention. Plasma levels of amyloid-? (A?) peptides have been a principal focus of the growing literature on blood-based biomarkers, but studies to date have varied in design, assay methods, and sample size, making it difficult to readily interpret the overall data.To conduct a systematic review and meta-analysis of relevant prospective studies to determine whether plasma amyloid-? levels may predict development of dementia, AD, and cognitive decline.We searched prospective studies published between 1995 and 2011 indexed in the MEDLINE, EMBASE, and PsycINFO databases. Selected studies included those measuring at least 1 relevant plasma amyloid-? species (A?(40), A?(42), or A?(42):A?(40) ratio) and reporting an effect estimate for dementia, AD, or cognitive change.Using a standardized extraction form, appropriate study parameters on subject information, exposure, and outcome were extracted. Random effects models were used to generate summary risk ratios and 95% confidence intervals comparing the bottom vs top quantiles for each plasma measure.Thirteen studies with a total of 10 303 subjects met inclusion criteria for meta-analysis. Lower A?(42):A?(40) ratios were significantly associated with development of AD (summary risk ratio, 1.60; 95% CI, 1.04-2.46; P = .03) and dementia (risk ratio, 1.67; 95% CI, 1.02-2.75; P = .04). Significant heterogeneity was found for both summary estimates, which could not be explained by participants' age, sex distribution, the study's follow-up time, or year of publication. Plasma levels of A?(40) and A?(42) alone were not significantly associated with either outcome.Overall, the literature indicates that plasma A?(42):A?(40) ratios predict development of AD and dementia. However, significant heterogeneity in the meta-analysis underlines the need for substantial further investigation of plasma amyloid-? levels as a preclinical biomarker.
| S-EPMC3772635 | biostudies-literature
Project description:Hypothyroidism is the most frequent consequence of the interaction of a large variety of drugs, environmental pollutants and industrial chemicals with the thyroid gland. It is associated with diminished endocrine function which may lead to hyperlipidemia, diabetes, Alzheimer's disease, weight gain, and other metabolic disorders. The present study evaluates the pro-thyroid activity of a bioactive fraction from a polyherbal teabag in rats with hypothyroidism induced by propylthiouracil. The teabag was formulated to stimulate synthesis and/or release of T4 and affectthe conversion of T4 to T3. Phytoconstituents of the polyherbal teabag are potent antioxidants that may be responsible for the pro-thyroid activity. The tea-extract (1000?mg) was found to contain 1076 ?g of gallic acid and 1131 ?g of rutin from HPTLC analysis. Rats received propylthiouracil (8?mg/kg) for the first 15days followed by the polyherbal tea-extract (500, 1000 and 1500?mg/kg), the standard drug levothyroxine (0.1?mg/kg), aerobic exercise, and a combination of tea-extract (1000?mg/kg) and aerobic exercise daily along with propylthiouracil for the next 30 days. Finally, rats received their respective treatments alone without propylthiouracil for 15 more days. Lipid profile and levels of glucose, insulin, T3, T4, TSH, cortisol, homocysteine, creatinine, uric acid, malondialdehyde, glucose-6 phosphatase, and endogenous antioxidants were determined. All treatments attenuated significantly the propylthiouracil-elevated TSH, homocysteine, creatinine, uric acid, glucose-6-phosphatase, insulin, and malondialdehyde levels, and restored favorably the propylthiouracil-altered lipid profile, T3, T4, and endogenous antioxidant levels. The polyherbal tea-extract (1000 and 1500?mg/kg) treatment and thecombination treatment of tea-extract (1000?mg/kg) with aerobic exercise displayed significant restoration of the suboptimalthyroid function. This may be due to a favorablemodulation ofthe hypothalamic-pituitary-thyroid and the hypothalamic-pituitary-adrenal axes.
| S-EPMC7301176 | biostudies-literature
Project description:BackgroundBy 2050, it has been estimated that approximately one-fifth of the population will be made up of older adults (aged ≥60 years). Old age often comes with cognitive decline and dementia. Physical activity may prevent cognitive decline and dementia.MethodsWe reviewed and synthesised prospective studies into physical activity and cognitive decline, and physical activity and dementia, published until January 2014. Forty-seven cohorts, derived from two previous systematic reviews and an updated database search, were used in the meta-analyses. Included participants were aged ≥40 years, in good health and/or randomly selected from the community. Studies were assessed for methodological quality.ResultsTwenty-one cohorts on physical activity and cognitive decline and twenty-six cohorts on physical activity and dementia were included. Meta-analysis, using the quality-effects model, suggests that participants with higher levels of physical activity, when compared to those with lower levels, are at reduced risk of cognitive decline, RR 0.65, 95% CI 0.55-0.76, and dementia, RR 0.86, 95% CI 0.76-0.97. Sensitivity analyses revealed a more conservative estimate of the impact of physical activity on cognitive decline and dementia for high quality studies, studies reporting effect sizes as ORs, greater number of adjustments (≥10), and longer follow-up time (≥10 years). When one heavily weighted study was excluded, physical activity was associated with an 18% reduction in the risk of dementia (RR 0.82; 0.73-0.91).ConclusionsLongitudinal observational studies show an association between higher levels of physical activity and a reduced risk of cognitive decline and dementia. A case can be made for a causal interpretation. Future research should use objective measures of physical activity, adjust for the full range of confounders and have adequate follow-up length. Ideally, randomised controlled trials will be conducted. Regardless of any effect on cognition, physical activity should be encouraged, as it has been shown to be beneficial on numerous levels.
| S-EPMC4064273 | biostudies-literature