Active clinical trials for "Cognitive Dysfunction"

Meningioma are slow growing and frequently occurring intracranial tumors, responsible for 33% of all asymptomatic intracranial tumors and 13-26% of all symptomatic primary brain tumors. The 10-year survival rate is 72%. A variety of treatment options is available for symptomatic meningioma including surgical removal with or without radiotherapy or radiotherapy alone. These therapies can have negative impact on cerebral functioning. After high dose radiotherapy for primary or metastatic brain tumors 50-90% of > 6 months' survivors develop irreversible disabling cognitive decline leading to premature loss of independence, reduced Quality of Life (QOL) as well as significant economic burden both at the individual as societal level. Especially for patients with a good prognosis like benign meningioma, maintaining neurocognitive function is crucial. Understanding the mechanisms underlying radiation induced cognitive decline is complex and which brain areas to spare are an important subject of research. Evaluation methods to assess cognitive function and predict cognitive decline are urgently needed, this will allow the development of optimized treatment strategies with the aim to preserve or even improve cognitive function in meningioma patients. Improvements in the field of neuroimaging techniques (i.e. advanced MRI techniques) have the possibility to identify areas susceptible to cognitive impairment. This allows in the future a more personalized radiation treatment by identifying patients at risk, by optimizing the radiotherapy dose to specific brain regions, that could eventually reduce or prevent, cognitive decline. Improvements in the field of radiotherapy for example by higher precision treatment such proton therapy have potential in obtaining these more individualized strategies.

A longitudinal observational neuroimaging study of individuals with Early Onset Alzheimer's disease during the prodromal phase, and matched control group - Ultrahigh Field MRI study at 7T

The purpose of this research study is to see how the brain changes in patients receiving chemotherapy (cytotoxic drug) treatment for colon or rectal cancer at Parkview Cancer Institute. This information will be used to identify helpful tests to diagnose individuals at risk for developing difficulties with thinking and memory due to their cancer treatments.

This study examines the association of variability in glucose values over a 10-day period with cognitive function and functional status among individuals with prediabetes, aged 50 or older.

This is a research study that aims to examine whether Veterans with mild Traumatic Brain Injuries are at risk for dementia by studying their memory, brain wave activity, brain structure and proteins that can be elevated after brain injury and in dementia.

The aim of the study is to assess a multidomain non-pharmacological intervention for improvement or maintenance of cognitive functioning and reduction of cognitive decline in the non-demented elderly from the general population. To investigate brain structural and functional imaging changes following a multidomain intervention. The recruited elderly aged 55-75 years with normal cognitive function or MCI will be divided into the intervention group or the control group randomly. The intervention group will be accepted a 6-week multidimensional non-pharmacological intervention (cognitive training, physical exercise, healthy lifestyle intervention, and computerized cognitive training) while the control group receives a 6-week health education. Sociodemographics will be collected before the intervention. comprehensive neuropsychological tests and MRI will be collected before and 6 weeks after the intervention respectively.

This is a multi-center longitudinal study that consists of five cohorts: cognitive normal aging (CN), Subjective cognitive impairment (SCI), mild cognitive impairment (MCI), Alzheimer's disease (AD) and vascular cognitive impairment (VCI). The goals of this study are as follow: 1.To establish longitudinal cohort study database containing comprehensive epidemiological data, neuropsychological test data, laboratory parameters, image data and biological samples. 2. To determine the risk factors of AD and other dementias. 3. To explore the conversion rates from CN to SCI, MCI or AD and the risk factors as well as biomarkers for the progression from CN to SCI, MCI or AD. 4. To explore and validate blood, CSF, urine, imaging and other biomarkers for the early detection and progression of AD.

The incidence of AD dementia is increasing due to the aging population, putting a heavy burden on our society and economics. Exploring the mechanisms underlying SCD due to preclinical AD has scientific and clinical significance. However, it is challenging to construct and validate the preclinical diagnosis model of AD with fused multimodel information across culture/race. From the cooperation during the past five years, we have established cohorts by synchronized assessment, achieved consensus on SCD features extraction and made a breakthrough in the application of multiple parameter MRI with German collaborators. Therefore, in this project, SCD with and without amyloid pathology will be compared by clinical and cognitive data, genetics, blood and MRI biomarkers between the German and Chinese. Key features will be extracted and specific characteristics of SCD due to preclinical AD as well as risk factors for conversion between two countries will be clarified. Then the diagnosis model of preclinical AD in SCD will be established across culture/race based on radiogenomics, which will improve the current diagnostic system of AD. Through this project, the value of SCD in the etiologic, anatomical and quantitative diagnosis of preclinical AD will be identified to improve sensitivity and specificity of preclinical AD diagnosis in clinical practice.

The purpose of this study is to identify genetic factors that contribute to or cause dementia (loss of memory) and related disorders across all ages and ethnic groups. This includes a number of neurological diseases such as early and late-onset Alzheimer disease, mild cognitive impairment, and other dementias.

Cognitive impairment is a common non-motor symptom among individuals living with Parkinson's disease (PD). Traditionally, cognitive impairment is thought to reflect disruptions in dopaminergic frontal-striatal systems. However, the current conceptualization does not thoroughly explain the heterogeneous profiles or trajectories of cognitive impairment in PD; suggesting that alternative mechanisms may contribute to cognitive impairments. Identification of alternative mechanisms of cognitive impairment may lead to better prognostic prediction and yield novel treatment targets. The gut is implicated as a site of early pathology in PD. Early signs of PD pathology (alpha synuclein and Lewy body aggregates) are detected in the gastrointestinal tract years before motor symptoms manifest. Recent studies provide evidence that individuals with PD have an altered gut-bacterial composition (termed dysbiosis) relative to controls. To date, dysbiosis is linked to more severe motor symptoms and certain non-motor symptoms (constipation, REM behavioral sleep disorder) in PD, but the relationship between dysbiosis and cognitive impairment remains unknown. Animal studies support the hypothesis that microbiota composition play a direct role in cognitive impairment. Germ free (GF) mice demonstrate deficits in cognition. Specifically, findings suggest that a disrupted gut- microbial environment in conjunction with elevated stress hormones may create an imbalance of pro- inflammatory vs. anti-inflammatory cytokines that induces potentially reversible cognitive impairments. In human studies among individuals with PD, neuroinflammatory markers are associated with cognitive impairment. However, the relationship between dysbiosis, neural inflammation and cognitive functioning remains unknown. This model has incredible clinical implications, as microbiota dysbiosis may represent a reversible risk factor for cognitive impairment. The proposed study will examine the hypothesis that dysbiosis contributes to increased neuroinflammation and cognitive impairment. Microbiota composition/function, neuroinflammatory markers and cognitive functioning will be examined in 100 participants with PD. Analyses of microbiota composition/function will examine abundance of amplicon sequence variants (ASVs; 16s), bacterial species/strains (metagenomics), microbial genes, and functional pathways. We hypothesize that microbiota composition/function will be associated with inflammatory markers (e.g. interleukin-6, tumor necrosis factor-alpha, c-reactive protein) and cognitive impairment.