SEARCH · Search PubMed

Results for “Critical Pathways”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 613 records · Page 34Linked to original sources

PubMed1985

Radiological impact assessment of an abandoned radium salts factory.

A radiological assessment has been in progress, since 1978, on the environmental implications of an abandoned radium salts factory, operating in Portugal from 1912 to 1944. Some aspects of the study performed at the site are briefly described. They include the analysis of radium-226 concentrations in water and foodstuff and the identification of critical pathways. The resulting dose equivalents due to radium intake and external irradiation are evaluated for the two most exposed groups of the population, and compared with values from other regions. Their sensitivity to some of the factors assumed is also discussed.

Adult↗

PubMed1987

Sources and behavior of technetium in the environment.

Technetium is a man-made element produced in increasing amounts during the last decades. The chemical and physical properties of some technetium compounds are considered, and a discussion of possible source terms is included. Literature on the environmental behavior of technetium is reviewed to evaluate its transfer and equilibrium distribution in aquatic and terrestrial ecosystems. Considerable effort has been expended in the last years in order to understand the biogeochemical processes responsible for the long-term behavior of technetium in the environment and its transfer through food chains as well as to identify critical pathways of the long-lived radioisotope Tc-99 from the environment to man.

Environmental Pollution↗

PubMed1993

Deficient expression of a B cell cytoplasmic tyrosine kinase in human X-linked agammaglobulinemia.

We describe a novel cytoplasmic tyrosine kinase, termed BPK (B cell progenitor kinase), which is expressed in all stages of the B lineage and in myeloid cells. BPK has classic SH1, SH2, and SH3 domains, but lacks myristylation signals and a regulatory phosphorylation site corresponding to tyrosine 527 of c-src. BPK has a long, basic amino-terminal region upstream of the SH3 domain. BPK was evaluated as a candidate for human X-linked agammaglobulinemia (XLA), an inherited immunodeficiency characterized by a severe deficit of B and plasma cells and profound hypogammaglobulinemia. BPK mapped to within 100 kb of a probe defining the polymorphism most closely linked to XLA at DXS178. Reduction in or the absence of BPK mRNA, protein expression, and kinase activity was observed in XLA pre-B and B cell lines. BPK is likely the XLA gene and functions in pathways critical to B cell expansion.

Agammaglobulinemia↗

PubMed1995

Role of metabolism in ethyl carbamate-induced suppression of antibody response to sheep erythrocytes in female Balb/C mice.

A possible role of metabolism by cytochrome P450 (P450) in ethyl carbamate-induced suppression of the antibody response to a T-cell-dependent antigen, sheep erythrocytes (SRBCs), was investigated in female Balb/C mice. When mice were treated with ethyl carbamate intraperitoneally for 14 consecutive days at 25, 50, 100, 200 and 400 mg/kg, the antibody response was significantly suppressed from 200 mg/kg. These doses also caused a decrease in thymus weight. An acute dosing of ethyl carbamate at 1 g/kg also caused not only a significant suppression of the antibody response, but also a decrease in thymus weight. The antibody response was most likely to be the IgM antibody response, which was demonstrated in a haemagglutination study. When mice were pretreated with phenobarbital (80 mg/kg) for 3 days to induce P450 enzymes, followed by administration of ethyl carbamate intraperitoneally for 7 consecutive days, the antibody response was more suppressed than in saline-pretreated controls. Moreover, a study using aminoacetonitrile, a P450 inhibitor, showed that the antibody response suppressed by ethyl carbamate was completely recovered by the inhibitor. The present results suggest that metabolism of ethyl carbamate by P450 may be the critical pathway to produce metabolites capable of suppressing the antibody response.

Animals↗

PubMed1984

Ecoepidemiology--a casuistic discipline describing ecological disturbances and damages in relation to their specific causes: exemplified by chlorinated phenols and chlorophenoxy acids.

Ecoepidemiology is a new concept created in analogy to human epidemiology, and aims at the study of ecotoxicological effects at the levels of ecosystems, biological communities, and populations in relation to causative environmental exposures, mostly by chemicals. By way of example, ecoepidemiology is described by presenting an example of unintentional dissipation and possible discharges of chlorophenols and phenoxy acids into the terrestrial environment and--as a more specific case--a marine, aquatic area, viz., the Køge Bay immediately to the south of Copenhagen, Denmark. The examples are illustrative of the complex situation which characterizes most ecoepidemiological cases. Difficulties with which the ecoepidemiologist are confronted are not only the identification of possible causative and confounding chemicals, and the description of ecoepidemiological effects per se, but also the assessment of critical pathways of multimedium pollutants. Biomonitoring, computer-based handling of data from natural localities, and determination of a variety of anthropogenic impact factors are necessary elements of ecoepidemiological studies.

Animals↗

PubMed1994

Outflow from the nucleus accumbens to the pedunculopontine tegmental nucleus: a dissociation between locomotor activity and the acquisition of responding for conditioned reinforcement stimulated by d-amphetamine.

Output of neuronal information from the nucleus accumbens to the ventral pallidum is known to be a critical pathway in the expression of locomotion and incentive-related behaviour. Some signals from this structure are relayed forward through the dorsomedial nucleus of the thalamus to the medial prefrontal cortex, but the other major pathway from this site is a descending innervation to the pedunculopontine tegmental nucleus. Information carried by these descending neurons has been linked with both the output of locomotor activity and incentive-related information. Previous studies carried out in this laboratory have shown no changes in locomotor activity--either spontaneous or in response to systemic administration of d-amphetamine or apomorphine--in rats with excitotoxic lesions of the pedunculopontine tegmental nucleus. The present experiments compare the effects of ibotenate lesions of this nucleus in tests of locomotor activity or the acquisition of responding with conditioned reinforcement, following injections of d-amphetamine directly into the nucleus accumbens. In general agreement with previous results, ibotenate lesions of the pedunculopontine tegmental nucleus did not alter locomotion stimulated directly from the nucleus accumbens. However, comparable lesions in a group of trained rats produced an array of deficits in the conditioned reinforcement paradigm. Most notably, these rats directed their attention almost entirely towards pressing the levers (practically ignoring the food-hopper panel), but did not appear to be able to discriminate between them, while controls focused almost all their efforts on pressing the reinforcing lever (virtually ignoring the non-reinforcing lever) and the food-hopper panel. These results indicate that pedunculopontine tegmental nucleus lesions disrupt an element of reward-related responding, but do not affect the production of locomotor activity. This highlights the unlikely existence of specific "locomotion-inducing" centres in the mesencephalon and implicates the pedunculopontine tegmental nucleus in the formation of stimulus-reward associations. These data are discussed with respect to a role for the pedunculopontine tegmental nucleus in response selection.

Animals↗

PubMed2004

Activation of epidermal growth factor receptor via CCR3 in bronchial epithelial cells.

We have previously found that bronchial epithelial cells express CCR3 whose signaling elicits mitogen-activated protein (MAP) kinase activation and cytokine production. Several investigators have focused on the signaling crosstalk between G protein-coupled receptors (GPCRs) and epidermal growth factor receptor (EGFR) in cancer cells. In this study, we investigated the role of EGFR in CCR3 signaling in the bronchial epithelial cell line NCI-H292. Eotaxin (1-100 nM) induced dose-dependent tyrosine phosphorylation of EGFR in NCI-H292 cells. Pretreatment of the cells with the EGFR inhibitor (AG1478) significantly inhibited the MAP kinase phosphorylation induced by eotaxin. Eotaxin stimulated IL-8 production, which was inhibited by AG1478. The transactivation of EGFR through CCR3 is a critical pathway that elicits MAP kinase activation and cytokine production in bronchial epithelial cells. The delineation of the signaling pathway of chemokines will help to develop a new therapeutic strategy to allergic diseases including bronchial asthma.

Bronchi↗

PubMed2006

Chondroitin sulfate A chains enhance platelet derived growth factor-mediated signalling in fibrosarcoma cells.

Platelet derived growth factor is involved in the autocrine growth stimulation of malignant cells, the stimulation of angiogenesis and the recruitment and regulation of tumor fibroblasts. PDGF has been shown to physically interact with glycosaminoglycans which are abundant in the fibrosarcoma cell microenvironment. Aim of the present study was to examine the effects of glycosaminoglycans on the mitogenic function of platelet derived growth factor in two human fibrosarcoma cell lines (B6FS, HT1080). For this purpose exogenously added glycosaminoglycans, regulators of endogenous glycosaminoglycan synthesis (sodium chlorate as selective inhibitor and beta-D-xyloside as a stimulator) and specific glycosidases to cleave cell-associated glycosaminoglycans, were utilized. Platelet derived growth factor demonstrated a growth stimulating effect on B6FS, whereas no effect was evident on HT1080 fibrosarcoma cells. Beta-D-xyloside had no effect on the basal level or the platelet derived growth factor-induced cell proliferation, whereas sodium chlorate severely reduced the basal level of proliferation in both cell lines. Significant co-stimulatory effects of chondroitin sulfate A in combination with platelet derived growth factor BB on the growth of HT1080 and B6FS cells were found. The co-stimulatory effect of chondroitin sulfate A was not due to transcriptional up regulation of platelet derived growth factor receptors genes, but rather to more efficient signalling of tyrosine kinase receptors. In conclusion, this study shows that chondroitin sulfate A can enhance the mitogenic activity of platelet-derived growth factor in fibrosarcoma cells utilizing a pathway which involves tyrosine kinases. This result introduces a new modulating role for chondroitin sulfate in signalling pathways critical for cancer growth.

Becaplermin↗

PubMed2005

Point-of-Care Testing and Cardiac Biomarkers: The Standard of Care and Vision for Chest Pain Centers.

Point-of-care testing (POCT) is defined as testing at or near the site of patient care. POCTdecreases therapeutic turnaround time (TTAT), increases clinical efficiency, and improves medical and economic outcomes. TTAT represents the time from test ordering to patient treatment. POC technologies have become ubiquitous in the United States, and, therefore,so has the potential for speed, convenience, and satisfaction, strong advantages for physicians, nurses, and patients in chest pain centers. POCT is applied most beneficially through the collaborative teamwork of clinicians and laboratorians who use integrative strategies, performance maps, clinical algorithms, and care paths (critical pathways). For example, clinical investigators have shown that on-site integration of testing for cardiac injury markers (myoglobin, creatinine kinase myocardial band [CKMB],and cardiac troponin I [cTnI]) in accelerated diagnostic algorithms produces effective screening, less hospitalization, and substantial savings. Chest pain centers, which now total over 150 accredited in the United States, incorporate similar types of protocol-driven performance enhancements. This optimization allows chest pain centers to improve patient evaluation, treatment, survival, and discharge. This article focuses on cardiac biomarker POCT for chest pain centers and emergency medicine.

Acute Disease↗

PubMed2006

Transcriptional repression of PGC-1alpha by mutant huntingtin leads to mitochondrial dysfunction and neurodegeneration.

Huntington's disease (HD) is an inherited neurodegenerative disease caused by a glutamine repeat expansion in huntingtin protein. Transcriptional deregulation and altered energy metabolism have been implicated in HD pathogenesis. We report here that mutant huntingtin causes disruption of mitochondrial function by inhibiting expression of PGC-1alpha, a transcriptional coactivator that regulates several metabolic processes, including mitochondrial biogenesis and respiration. Mutant huntingtin represses PGC-1alpha gene transcription by associating with the promoter and interfering with the CREB/TAF4-dependent transcriptional pathway critical for the regulation of PGC-1alpha gene expression. Crossbreeding of PGC-1alpha knockout (KO) mice with HD knockin (KI) mice leads to increased neurodegeneration of striatal neurons and motor abnormalities in the HD mice. Importantly, expression of PGC-1alpha partially reverses the toxic effects of mutant huntingtin in cultured striatal neurons. Moreover, lentiviral-mediated delivery of PGC-1alpha in the striatum provides neuroprotection in the transgenic HD mice. These studies suggest a key role for PGC-1alpha in the control of energy metabolism in the early stages of HD pathogenesis.

Animals↗

PubMedDate not supplied

How do we get fat? An epidemiologic and metabolic approach.

Obesity results when the energy intake exceeds expenditure for a long period. The first law of thermodynamics, which describes this relationship, does not provide insight into the failures to couple energy intake and expenditure. Research over the past two decades has provided an unprecedented expansion of knowledge about the physiological and molecular mechanisms regulating body fat. Perhaps the greatest impact has resulted from the cloning of genes corresponding to the five mouse monogenic obesity syndromes and the subsequent characterization of the human counterparts to these syndromes. Extensive molecular and reverse genetic studies (mouse knockouts) have helped establish other critical pathways that regulate body fat and food intake, and also have either validated or refuted the importance of previously identified pathways.

Adipocytes↗

PubMed2004

Controlling the balance between osteoblastogenesis and adipogenesis and the consequent therapeutic implications.

The increase in marrow adipogenesis associated with osteoporosis and age-related osteopenia is well known clinically. However, we are only now beginning to understand the mechanisms that control the differentiation of mesenchymal stem cells to either osteoblasts or adipocytes. Recent work with gene silencing and overexpression has provided insight into critical pathways that determine the fate of these multipotential cells. One of these pathways - that of the nuclear hormone receptor peroxisome proliferator activated receptor-gamma - when activated, promotes adipogenesis and inhibits osteogenesis. This in vitro mechanism of action has been confirmed in vivo using ligands to this receptor. Discovery of this and other targets and pathways, such as Wnt signaling, notch/delta/jagged ligands and receptors, and RhoA gene expression, provides new insights into mesenchymal stem cell differentiation. These pathways provide exciting future pharmacological targets with which to enhance bone formation and therefore reduce the risk of fracture.

Adipocytes↗

PubMed2006

C. elegans FANCD2 responds to replication stress and functions in interstrand cross-link repair.

One of the least well understood DNA repair processes in cells is the repair of DNA interstrand cross-links (ICLs) which present a major obstacle to DNA replication and must be repaired or bypassed to allow fork progression. Fanconi anemia (FA) is an inherited genome instability syndrome characterized by hypersensitivity to ICL damage. Central to the FA repair pathway is FANCD2 that is mono-ubiquitylated in response to replication stress and ICL damage through the action of the FA core complex and its E3-ubiquitin ligase subunit, FANCL. In its mono-ubiquitylated form FANCD2 is recruited to repair foci where it is believed to somehow coordinate ICL repair and restart of impeded replication forks. However, the precise mechanism through which the FA pathway and mono-ubiquitylation of FANCD2 promotes ICL repair remains unclear. Here we report on a functional homologue of FANCD2 in C. elegans (FCD-2). Although fcd-2 mutants are homozygous viable, they are exquisitely sensitive to ICL-inducing agents, but insensitive to ionizing radiation (IR). fcd-2 is dispensable for meiotic recombination and activation of the S-phase checkpoint, indicating that ICL sensitivity is likely due to a repair rather than a signalling defect. Indeed, we show that FCD-2 is mono-ubiquitylated in response to ICL damage and is recruited to nuclear repair foci. Consistent with the sensitivity of fcd-2 mutants, FCD-2 focus formation is induced in response to ICL damage and replication stress, but not following IR, suggesting that FCD-2 responds to lesions that block DNA replication and not DNA double strand breaks per se. The realization that the FA pathway is conserved in a genetically tractable model system will permit the comprehensive analysis of the interplay between the FA, homologous recombination (HR), translesion synthesis (TLS) and nucleotide excision repair (NER) pathways, critical to the understanding of ICL repair.

Amino Acid Sequence↗

PubMed2004

Severity scoring in community-acquired pneumonia caused by Streptococcus pneumoniae: a 5-year experience.

Multiple severity scoring systems have been devised and evaluated in community-acquired pneumonia (CAP), but a simplified set of prognostic indicators has not yet been developed. Streptococcus pneumoniae is the most frequent aetiological agent of CAP. Our aim was to characterise the outcome in the light of different severity scoring systems and to compare the predictive values of different sets of clinical parameters, using available clinical data for pneumococcal CAP patients. This is a case series retrospective analysis that included consecutive adult pneumococcal CAP patients admitted to Danbury Hospital between 1 January 1996 and 31 December 2000. The aetiology was confirmed by positive sputum and/or blood cultures. The severity assessment included the Pneumonia Outcome Research Trial (PORT) and British Thoracic Society (BTS) scoring systems and other additional parameters. Primary end-points were in-hospital CAP-attributable deaths and length of hospitalisation. N = 151 patients with S. pneumoniae CAP were identified. The mean (+/- standard deviation) age at the time of diagnosis was 68 (+/-15) years. Thirty-three patients (22%) were admitted to the medical intensive care unit. The mean (median) hospitalisation duration was 7.5 (+/-5) days. Door-to-antibiotic mean (median) administration time was 3.7 (2) hours. Most frequent antibiotics used initially were cephalosporins plus/minus macrolides or fluoroquinolones. The mean (+/- standard deviation) PORT score was 105 (+/-37). The observed CAP-related mortality was 9/151 (5.9%, 95% confidence interval: 3-9%). The mortality rate in ICU was 18% (6/33). Sixty-nine patients (45%) had S. pneumoniae bacteraemia an admission. The bacteraemic and non-bacteraemic patients had similar PORT scores (107 vs. 104, P = 0.66), length of hospitalisation (8 vs. 7 days, P = 0.41) and mortality rates (9% vs. 4%, P = 0.30). In conclusion, patients admitted with pneumococcal CAP, although severe and with multiple co-morbidities had low in-hospital mortality rates and lengths of hospitalisation. Neither prior antimicrobial use (or failure) nor antimicrobial resistance contributed to an adverse outcome. S. pneumoniae bacteraemia failed to correlate with need for ICU, length of stay, higher morbidity index or fatal outcome. Low rates of empirical antibiotic use for non-bacterial infections in the local community, implementation of an emergency department protocol for CAP therapy, early recognition of higher risk patients and placement in ICU, use of broad spectrum antibiotics, infectious disease approval or critical pathway restriction for admission orders, could all have combined to effect a good outcome for these patients.

Aged↗

PubMed2026

Pragmatic gynecologic cancer clinical trials: statements and roadmap from the Gynecologic Cancer InterGroup Chicago Brainstorming Meeting.

Randomized controlled trials remain fundamental to evidence generation in oncology but are increasingly complex, costly, and often misaligned with real-world practice. Traditional explanatory trials, designed under ideal, controlled conditions, frequently enroll highly selected populations, limiting generalizability and underrepresenting key groups such as older adults, patients with comorbidities, and those from low- and middle-income countries. Pragmatic clinical trials offer an alternative by evaluating interventions under routine care conditions, with broader eligibility, simplified procedures, and patient-centered outcomes. To address these challenges, the Gynecologic Cancer InterGroup convened an international brainstorming meeting in May 2025 with multi-disciplinary experts, patients, and advocates to define priorities and develop a roadmap for pragmatic trials in gynecologic oncology. Key discussions emphasized embedding trial design within routine care, aligning eligibility criteria and procedures with standard practice, minimizing non-essential data collection, and prioritizing outcomes meaningful to patients, including quality of life. Innovative designs such as registry-based randomized trials, trials-within-cohorts, and cluster randomization were highlighted as feasible approaches to improve efficiency while preserving internal validity. Integration of patient-reported outcomes and real-world data was considered achievable when carefully streamlined. Major challenges identified included regulatory heterogeneity, consent complexity, data interoperability, and funding limitations, particularly in multi-national settings. Proposed solutions include simplified consent models, centralized ethics processes, hybrid funding strategies, and the responsible use of artificial intelligence to enhance patient identification, recruitment, and potential development of synthetic control arms. Patient engagement was recognized as essential to ensure relevance, feasibility, and equity. Incorporation of patient-reported outcomes was discussed as key to informing acceptance and tolerability. In summary, pragmatic trials within Gynecologic Cancer InterGroup represent a critical pathway to generate efficient, inclusive, and practice-changing evidence in gynecologic cancers across diverse health care settings.

Humans↗

PubMed2005

Mechanisms of nutrient modulation of the immune response.

Lack of adequate macronutrients or selected micronutrients, especially zinc, selenium, iron, and the antioxidant vitamins, can lead to clinically significant immune deficiency and infections in children. Undernutrition in critical periods of gestation and neonatal maturation and during weaning impairs the development and differentiation of a normal immune system. Infections are both more frequent and more often become chronic in the malnourished child. Recent identification of genetic mechanisms is revealing critical pathways in the gastrointestinal immune response. New studies show that the development of tolerance, control of inflammation, and response to normal mucosal flora are interrelated and linked to specific immune mechanisms. Nutrients act as antioxidants and as cofactors at the level of cytokine regulation. Protein calorie malnutrition and zinc deficiency activate the hypothalamic-pituitary-adrenal axis. Increased circulating levels of glucocorticoids cause thymic atrophy and affect hematopoiesis. Chronic undernutrition and micronutrient deficiency compromise cytokine response and affect immune cell trafficking. The combination of chronic undernutrition and infection further weakens the immune response, leading to altered immune cell populations and a generalized increase in inflammatory mediators. Obesity caused by excess nutrition or excess storage of fats relative to energy expenditure is a form of malnutrition that is increasingly seen in children. Leptin is emerging as a cytokine-like immune regulator that has complex effects in both overnutrition and in the inflammatory response in malnutrition. Because the immune system is immature at birth, malnutrition in childhood might have long-term effects on health.

Child↗

PubMed2005

Advances in understanding the molecular causes of diabetes-induced birth defects.

OBJECTIVE: To review the current understanding of the molecular causes of birth defects resulting from diabetic pregnancy, with a focus on neural tube defects. METHODS: A mouse model of diabetic pregnancy is described, in which embryo gene expression associated with neural tube defects is examined. Chemical, physiologic, or genetic manipulations are employed to elucidate critical pathways affected by increased glucose metabolism, and how abnormal gene expression disrupts neural tube closure. RESULTS: Increased glucose delivery to embryos, or activation of pathways that are stimulated by high glucose, such as the hexosamine biosynthetic pathway or hypoxia, increase oxidative stress in embryos, inhibit expression of Pax3, a gene that encodes a transcription factor that is required for neural tube closure, and increase neural tube defects. Conversely, blocking these pathways, or providing the antioxidants, reduced glutathione or vitamin E, suppress the adverse effects of excess glucose. Pax3 decreases steady-state levels of the p53 tumor-suppressor protein, such that when Pax3 is deficient, p53 protein increases, leading to increased neuroepithelial apoptosis prior to completion of neural tube closure. Embryos that lack both functional Pax3 protein and p53 do not display neuroepithelial apoptosis or neural tube defects. CONCLUSIONS: Excess glucose metabolism by embryos resulting from maternal hyperglycemia disturbs a complex network of biochemical pathways, leading to oxidative stress. Oxidative stress inhibits expression of genes, such as Pax3, which control essential developmental processes. Pax3 protein is required during neural tube development to suppress p53-dependent cell death and consequent abortion of neural tube closure, but is not required to control expression of genes that direct neural tube closure. Impaired embryo gene expression resulting from oxidative stress, and consequent apoptosis or disturbed organogenesis, may be a general mechanism to explain diabetic embryopathy.

Animals↗

PubMed2005

Contribution of the MTHFR gene to the causal pathway for depression, anxiety and cognitive impairment in later life.

Homocysteine (Hcy) is harmful to neurons and blood vessels, including the cerebral microvasculature. It is possible that such effects contribute to the cascade of events that leads to cognitive decline, dementia, and depression in later life. Hcy is produced during the metabolism of the essential amino-acid methionine, which also involves a methyl group transfer derived from folate and choline metabolism. Its plasma level can be influenced by factors such as age, vitamin deficiency, renal function, and a common mutation in the methylenetetrahydrofolate reductase (MTHFR) gene, where cytosine is replaced by thymidine (C-->T) at nucleotide position 677. Subjects with the TT genotype have higher homocysteine levels and may be particularly prone to experiencing depression as a result of high plasma Hcy and dysfunction of methylation metabolic pathways critical to the synthesis of noradrenaline and serotonin. We designed the present study to investigate whether older women with the TT genotype would have higher depression and lower cognitive scores than women with CT and CC genotypes. A total of 240 community-dwelling women aged 70 years or over volunteered to take part in the study - 29 carried the TT genotype, 113 the CT and 98 the CC genotype. The Beck Depression Inventory (BDI) score for subjects with the TT genotype was statistically similar to the other groups (P = 0.609). Plasma Hcy showed a modest and significant correlation with BDI scores (r = 0.21) that was independent from age, B12 and folate levels. There was no association between beck anxiety inventory (BAI) scores and MTHFR genotype or homocysteine levels. The cognitive assessment of participants included measures of verbal memory, memory for faces, verbal fluency, visuo-spatial abilities and the cognitive section of the Cambridge Examination For Mental Disorders Of The Elderly (CAMCOG)-MTHFR genotype had no clear association with cognitive scores. These results indicate that, in isolation, the MTHFR C677T gene variation does not play an important role in the modulation of mood and cognitive performance in later life.

Aged↗