19 results on '"Alosco, Michael L."'
Search Results
2. Neurodegenerative biomarkers in different chambers of the eye relative to plasma: an agreement validation study
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Sampani, Konstantina, Ness, Steven, Tuz-Zahra, Fatima, Aytan, Nurgul, Spurlock, Elizabeth E., Alluri, Sreevardhan, Chen, Xuejing, Siegel, Nicole H., Alosco, Michael L., Xia, Weiming, Tripodis, Yorghos, Stein, Thor D., and Subramanian, Manju L.
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- 2024
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3. Inflammatory biomarkers for neurobehavioral dysregulation in former American football players: findings from the DIAGNOSE CTE Research Project
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van Amerongen, Suzan, Pulukuri, Surya V., Tuz-Zahra, Fatima, Tripodis, Yorghos, Cherry, Jonathan D., Bernick, Charles, Geda, Yonas E., Wethe, Jennifer V., Katz, Douglas I., Alosco, Michael L., Adler, Charles H., Balcer, Laura J., Ashton, Nicholas J., Blennow, Kaj, Zetterberg, Henrik, Daneshvar, Daniel H., Colasurdo, Elizabeth A., Iliff, Jeffrey J., Li, Gail, Peskind, Elaine R., Shenton, Martha E., Reiman, Eric M., Cummings, Jeffrey L., and Stern, Robert A.
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- 2024
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4. Cognitive, functional, and neuropsychiatric correlates of regional tau pathology in autopsy-confirmed chronic traumatic encephalopathy
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Alosco, Michael L., White, Micaela, Bell, Carter, Faheem, Farwa, Tripodis, Yorghos, Yhang, Eukyung, Baucom, Zachary, Martin, Brett, Palmisano, Joseph, Dams-O’Connor, Kristen, Crary, John F., Goldstein, Lee E., Katz, Douglas I., Dwyer, Brigid, Daneshvar, Daniel H., Nowinski, Christopher, Cantu, Robert C., Kowall, Neil W., Stern, Robert A., Alvarez, Victor E., Huber, Bertrand Russell, Stein, Thor D., McKee, Ann C., and Mez, Jesse
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- 2024
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5. Amyloid PET across the cognitive spectrum in former professional and college American football players: findings from the DIAGNOSE CTE Research Project
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Stern, Robert A., Trujillo-Rodriguez, Diana, Tripodis, Yorghos, Pulukuri, Surya V., Alosco, Michael L., Adler, Charles H., Balcer, Laura J., Bernick, Charles, Baucom, Zachary, Marek, Kenneth L., McClean, Michael D., Johnson, Keith A., McKee, Ann C., Stein, Thor D., Mez, Jesse, Palmisano, Joseph N., Cummings, Jeffrey L., Shenton, Martha E., and Reiman, Eric M.
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- 2023
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6. Three dimensional evaluation of cerebrovascular density and branching in chronic traumatic encephalopathy
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Rosen, Grace, Kirsch, Daniel, Horowitz, Sarah, Cherry, Jonathan D., Nicks, Raymond, Kelley, Hunter, Uretsky, Madeline, Dell’Aquila, Kevin, Mathias, Rebecca, Cormier, Kerry A., Kubilus, Caroline A., Mez, Jesse, Tripodis, Yorghos, Stein, Thor D., Alvarez, Victor E., Alosco, Michael L., McKee, Ann C., and Huber, Bertrand R.
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- 2023
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7. Neuropsychological test performance of former American football players
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Alosco, Michael L., Barr, William B., Banks, Sarah J., Wethe, Jennifer V., Miller, Justin B., Pulukuri, Surya Vamsi, Culhane, Julia, Tripodis, Yorghos, Adler, Charles H., Balcer, Laura J., Bernick, Charles, Mariani, Megan L., Cantu, Robert C., Dodick, David W., McClean, Michael D., Au, Rhoda, Mez, Jesse, Turner, II, Robert W., Palmisano, Joseph N., Martin, Brett, Hartlage, Kaitlin, Cummings, Jeffrey L., Reiman, Eric M., Shenton, Martha E., and Stern, Robert A.
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- 2023
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8. A comparison between tau and amyloid-β cerebrospinal fluid biomarkers in chronic traumatic encephalopathy and Alzheimer disease
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Turk, Katherine W., Geada, Alexandra, Alvarez, Victor E., Xia, Weiming, Cherry, Jonathan D., Nicks, Raymond, Meng, Gaoyuan, Daley, Sarah, Tripodis, Yorghos, Huber, Bertrand R., Budson, Andrew E., Dwyer, Brigid, Kowall, Neil W., Cantu, Robert C., Goldstein, Lee E., Katz, Douglas I., Stern, Robert A., Alosco, Michael L., Mez, Jesse, McKee, Ann C., and Stein, Thor D.
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- 2022
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9. Structural MRI profiles and tau correlates of atrophy in autopsy-confirmed CTE
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Alosco, Michael L., Mian, Asim Z., Buch, Karen, Farris, Chad W., Uretsky, Madeline, Tripodis, Yorghos, Baucom, Zachary, Martin, Brett, Palmisano, Joseph, Puzo, Christian, Ang, Ting Fang Alvin, Joshi, Prajakta, Goldstein, Lee E., Au, Rhoda, Katz, Douglas I., Dwyer, Brigid, Daneshvar, Daniel H., Nowinski, Christopher, Cantu, Robert C., Kowall, Neil W., Huber, Bertrand Russell, Alvarez, Victor E., Stern, Robert A., Stein, Thor D., Killiany, Ronald J., McKee, Ann C., and Mez, Jesse
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- 2021
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10. CCL2 is associated with microglia and macrophage recruitment in chronic traumatic encephalopathy
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Cherry, Jonathan D., Meng, Gaoyuan, Daley, Sarah, Xia, Weiming, Svirsky, Sarah, Alvarez, Victor E., Nicks, Raymond, Pothast, Morgan, Kelley, Hunter, Huber, Bertrand, Tripodis, Yorghos, Alosco, Michael L., Mez, Jesse, McKee, Ann C., and Stein, Thor D.
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- 2020
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11. Variation in TMEM106B in chronic traumatic encephalopathy
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Cherry, Jonathan D., Mez, Jesse, Crary, John F., Tripodis, Yorghos, Alvarez, Victor E., Mahar, Ian, Huber, Bertrand R., Alosco, Michael L., Nicks, Raymond, Abdolmohammadi, Bobak, Kiernan, Patrick T., Evers, Laney, Svirsky, Sarah, Babcock, Katharine, Gardner, Hannah M., Meng, Gaoyuan, Nowinski, Christopher J., Martin, Brett M., Dwyer, Brigid, Kowall, Neil W., Cantu, Robert C., Goldstein, Lee E., Katz, Douglas I., Stern, Robert A., Farrer, Lindsay A., McKee, Ann C., and Stein, Thor D.
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- 2018
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12. Developing methods to detect and diagnose chronic traumatic encephalopathy during life: rationale, design, and methodology for the DIAGNOSE CTE Research Project.
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Alosco, Michael L., Mariani, Megan L., Adler, Charles H., Balcer, Laura J., Bernick, Charles, Au, Rhoda, Banks, Sarah J., Barr, William B., Bouix, Sylvain, Cantu, Robert C., Coleman, Michael J., Dodick, David W., Farrer, Lindsay A., Geda, Yonas E., Katz, Douglas I., Koerte, Inga K., Kowall, Neil W., Lin, Alexander P., Marcus, Daniel S., and Marek, Kenneth L.
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CHRONIC traumatic encephalopathy , *DIAGNOSIS , *MAGNETIC resonance imaging , *MEDICAL research , *POSITRON emission tomography , *NEUROLOGIC examination , *PSYCHIATRIC epidemiology - Abstract
Background: Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that has been neuropathologically diagnosed in brain donors exposed to repetitive head impacts, including boxers and American football, soccer, ice hockey, and rugby players. CTE cannot yet be diagnosed during life. In December 2015, the National Institute of Neurological Disorders and Stroke awarded a seven-year grant (U01NS093334) to fund the "Diagnostics, Imaging, and Genetics Network for the Objective Study and Evaluation of Chronic Traumatic Encephalopathy (DIAGNOSE CTE) Research Project." The objectives of this multicenter project are to: develop in vivo fluid and neuroimaging biomarkers for CTE; characterize its clinical presentation; refine and validate clinical research diagnostic criteria (i.e., traumatic encephalopathy syndrome [TES]); examine repetitive head impact exposure, genetic, and other risk factors; and provide shared resources of anonymized data and biological samples to the research community. In this paper, we provide a detailed overview of the rationale, design, and methods for the DIAGNOSE CTE Research Project. Methods: The targeted sample and sample size was 240 male participants, ages 45–74, including 120 former professional football players, 60 former collegiate football players, and 60 asymptomatic participants without a history of head trauma or participation in organized contact sports. Participants were evaluated at one of four U.S. sites and underwent the following baseline procedures: neurological and neuropsychological examinations; tau and amyloid positron emission tomography; magnetic resonance imaging and spectroscopy; lumbar puncture; blood and saliva collection; and standardized self-report measures of neuropsychiatric, cognitive, and daily functioning. Study partners completed similar informant-report measures. Follow-up evaluations were intended to be in-person and at 3 years post-baseline. Multidisciplinary diagnostic consensus conferences are held, and the reliability and validity of TES diagnostic criteria are examined. Results: Participant enrollment and all baseline evaluations were completed in February 2020. Three-year follow-up evaluations began in October 2019. However, in-person evaluation ceased with the COVID-19 pandemic, and resumed as remote, 4-year follow-up evaluations (including telephone-, online-, and videoconference-based cognitive, neuropsychiatric, and neurologic examinations, as well as in-home blood draw) in February 2021. Conclusions: Findings from the DIAGNOSE CTE Research Project should facilitate detection and diagnosis of CTE during life, and thereby accelerate research on risk factors, mechanisms, epidemiology, treatment, and prevention of CTE. Trial registration: NCT02798185 [ABSTRACT FROM AUTHOR]
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- 2021
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13. Microglial neuroinflammation contributes to tau accumulation in chronic traumatic encephalopathy.
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Cherry, Jonathan D., Tripodis, Yorghos, Alvarez, Victor E., Huber, Bertrand, Kiernan, Patrick T., Daneshvar, Daniel H., Mez, Jesse, Montenigro, Philip H., Solomon, Todd M., Alosco, Michael L., Stern, Robert A., McKee, Ann C., and Stein, Thor D.
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MICROGLIA ,CHRONIC traumatic encephalopathy ,TAU proteins ,THERAPEUTICS - Abstract
The chronic effects of repetitive head impacts (RHI) on the development of neuroinflammation and its relationship to chronic traumatic encephalopathy (CTE) are unknown. Here we set out to determine the relationship between RHI exposure, neuroinflammation, and the development of hyperphosphorylated tau (ptau) pathology and dementia risk in CTE. We studied a cohort of 66 deceased American football athletes from the Boston University- Veteran's Affairs-Concussion Legacy Foundation Brain Bank as well as 16 non-athlete controls. Subjects with a neurodegenerative disease other than CTE were excluded. Counts of total and activated microglia, astrocytes, and ptau pathology were performed in the dorsolateral frontal cortex (DLF). Binary logistic and simultaneous equation regression models were used to test associations between RHI exposure, microglia, ptau pathology, and dementia. Duration of RHI exposure and the development and severity of CTE were associated with reactive microglial morphology and increased numbers of CD68 immunoreactive microglia in the DLF. A simultaneous equation regression model demonstrated that RHI exposure had a significant direct effect on CD68 cell density (p < 0.0001) and ptau pathology (p < 0.0001) independent of age at death. The effect of RHI on ptau pathology was partially mediated through increased CD68 positive cell density. A binary logistic regression demonstrated that a diagnosis of dementia was significantly predicted by CD68 cell density (OR = 1.010, p = 0.011) independent of age (OR = 1.055, p = 0.007), but this effect disappeared when ptau pathology was included in the model. In conclusion, RHI is associated with chronic activation of microglia, which may partially mediate the effect of RHI on the development of ptau pathology and dementia in CTE. Inflammatory molecules may be important diagnostic or predictive biomarkers as well as promising therapeutic targets in CTE. [ABSTRACT FROM AUTHOR]
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- 2016
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14. Mini Mental State Examination and Logical Memory scores for entry into Alzheimer's disease trials.
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Chapman, Kimberly R., Bing-Canar, Hanaan, Alosco, Michael L., Steinberg, Eric G., Martin, Brett, Chaisson, Christine, Kowall, Neil, Tripodis, Yorghos, and Stern, Robert A.
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ALZHEIMER'S disease ,MINI-Mental State Examination ,CLINICAL trials ,MILD cognitive impairment ,NEURODEGENERATION - Abstract
Background: Specific cutoff scores on the Mini Mental State Examination (MMSE) and the Logical Memory (LM) test are used to determine inclusion in Alzheimer's disease (AD) clinical trials and diagnostic studies. These screening measures have known psychometric limitations, but no study has examined the diagnostic accuracy of the cutoff scores used to determine entry into AD clinical trials and diagnostic studies. Methods: ClinicalTrials.gov entries were reviewed for phases II and III active and recruiting AD studies using the MMSE and LM for inclusion. The diagnostic accuracy of MMSE and LM-II cutoffs used in AD trials and diagnostic studies was examined using 23,438 subjects with normal cognition, mild cognitive impairment (MCI), and AD dementia derived from the National Alzheimer's Coordinating Center database. Results: MMSE and LM cutoffs used in current AD clinical trials and diagnostic studies had limited diagnostic accuracy, particularly for distinguishing between normal cognition and MCI, and MCI from AD dementia. The MMSE poorly discriminated dementia stage. Conclusions: The MMSE and LM may result in inappropriate subject enrollment in large-scale, multicenter studies designed to develop therapeutics and diagnostic methods for AD. [ABSTRACT FROM AUTHOR]
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- 2016
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15. Reduced cerebral blood flow and white matter hyperintensities predict poor sleep in heart failure.
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Alosco, Michael L., Brickman, Adam M., Spitznagel, Mary Beth, Griffith, Erica Y., Narkhede, Atul, Cohen, Ronald, Sweet, Lawrence H., Hughes, Joel, Rosneck, Jim, and Gunstad, John
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HEART failure , *SLEEP disorders , *CEREBRAL circulation , *WHITE matter (Nerve tissue) , *PERFUSION , *REGRESSION analysis - Abstract
Background Poor sleep is common in heart failure (HF), though mechanisms of sleep difficulties are not well understood. Adverse brain changes among regions important for sleep have been demonstrated in patients with HF. Cerebral hypoperfusion, a correlate of sleep quality, is also prevalent in HF and a likely contributor to white matter hyperintensities (WMH). However, no study to date has examined the effects of cerebral blood flow, WMH, and brain volume on sleep quality in HF. Methods Fifty-three HF patients completed the Pittsburgh Sleep Quality Index and underwent brain magnetic resonance imaging to quantify brain and WMH volume. Transcranial Doppler ultrasonography assessed cerebral blood flow velocity of the middle cerebral artery (CBF-V of the MCA). Results 75.5% of HF patients reported impaired sleep. Regression analyses adjusting for medical and demographic factors showed decreased CBF-V of the MCA and greater WMH volume were associated with poor sleep quality. No such pattern emerged on total brain or regional volume indices. Conclusions Decreased cerebral perfusion and greater WMH may contribute to sleep difficulties in HF. Future studies are needed to confirm these findings and clarify the effects of cerebral blood flow and WMH on sleep in healthy and patient samples. [ABSTRACT FROM AUTHOR]
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- 2013
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16. Cognitive deficits are associated with poorer simulated driving in older adults with heart failure.
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Alosco, Michael L., Spitznagel, Mary Beth, Cleveland, Mary Jo, and Gunstad, John
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COGNITION disorders ,HEART failure patients ,OLDER people ,AUTOMOBILE driving ,EXECUTIVE function ,MINI-Mental State Examination ,DRIVING cessation - Abstract
Background: Cognitive impairment is prevalent in older adults with heart failure (HF) and associated with reduced functional independence. HF patients appear at risk for reduced driving ability, as past work in other medical samples has shown cognitive dysfunction to be an important contributor to driving performance. The current study examined whether cognitive dysfunction was independently associated with reduced driving simulation performance in a sample of HF patients. Methods: 18 persons with HF (67.72; SD = 8.56 year) completed echocardiogram and a brief neuropsychological test battery assessing global cognitive function, attention/executive function, memory and motor function. All participants then completed the Kent Multidimensional Assessment Driving Simulation (K-MADS), a driving simulator scenario with good psychometric properties. Results: The sample exhibited an average Mini Mental State Examination (MMSE) score of 27.83 (SD = 2.09). Independent sample t-tests showed that HF patients performed worse than healthy adults on the driving simulation scenario. Finally, partial correlations showed worse attention/executive and motor function were independently associated with poorer driving simulation performance across several indices reflective of driving ability (i.e., centerline crossings, number of collisions, % of time over the speed limit, among others). Conclusion: The current findings showed that reduced cognitive function was associated with poor simulated driving performance in older adults with HF. If replicated using behind-the-wheel testing, HF patients may be at elevated risk for unsafe driving and routine driving evaluations in this population may be warranted. [ABSTRACT FROM AUTHOR]
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- 2013
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17. Cardiovascular fitness associated with cognitive performance in heart failure patients enrolled in cardiac rehabilitation.
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Garcia, Sarah, Alosco, Michael L., Spitznagel, Mary Beth, Cohen, Ronald, Raz, Naftali, Sweet, Lawrence, Josephson, Richard, Hughes, Joel, Rosneck, Jim, Oberle, Morgan L., and Gunstad, John
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HEART failure ,CARDIOVASCULAR fitness ,METABOLIC equivalent ,COGNITIVE ability ,PHYSICAL fitness - Abstract
Background: Reduced cognitive function is common in persons with heart failure (HF). Cardiovascular fitness is a known contributor to cognitive function in many patient populations, but has only been linked to cognition based on estimates of fitness in HF. The current study examined the relationship between fitness as measured by metabolic equivalents (METs) from a standardized stress test and cognition in persons with HF, as well as the validity of office-based predictors of fitness in this population. Methods: Forty-one HF patients enrolled in cardiac rehabilitation completed a standardized exercise stress test protocol, a brief neuropsychological battery, the 2-minute step test (2MST), and a series of medical history and self-report questionnaires. Results: Maximum METs from stress testing demonstrated incremental predictive validity for attention (β = .41, p = .03), executive function (β = .37, p = .04), and memory domains (β = .46, p = .04). Partial correlations accounting for key medical and demographic characteristics revealed greater METs was associated with the 2MST (r (32) = .41, p = .02) but not with the Duke Activity Status Index (DASI) (r(32) = .24, p = .17). Conclusion: The current findings indicate that better fitness levels measured by METs is independently associated with better cognitive function in older adults with HF. Results also showed that METs was closely associated with one officebased measure of fitness (2MST), but not another (DASI). Prospective studies are needed to clarify the mechanisms linking fitness and cognitive function in HF. [ABSTRACT FROM AUTHOR]
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- 2013
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18. Independent effects of white matter hyperintensities on cognitive, neuropsychiatric, and functional decline: a longitudinal investigation using the National Alzheimer's Coordinating Center Uniform Data Set.
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Puzo, Christian, Labriola, Caroline, Sugarman, Michael A., Tripodis, Yorghos, Martin, Brett, Palmisano, Joseph N., Steinberg, Eric G., Stein, Thor D., Kowall, Neil W., McKee, Ann C., Mez, Jesse, Killiany, Ronald J., Stern, Robert A., and Alosco, Michael L.
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CEREBRAL small vessel diseases ,MILD cognitive impairment ,ALZHEIMER'S disease ,NEUROPSYCHOLOGICAL tests ,WHITE matter (Nerve tissue) ,COGNITION - Abstract
Background: Longitudinal investigations are needed to improve understanding of the contributions of cerebral small vessel disease to the clinical manifestation of Alzheimer's disease, particularly in the early disease stages. This study leveraged the National Alzheimer's Coordinating Center Uniform Data Set to longitudinally examine the association between white matter hyperintensities and neuropsychological, neuropsychiatric, and functional decline among participants with normal cognition. Methods: The sample included 465 participants from the National Alzheimer's Coordinating Center Uniform Data Set who had quantitated volume of white matter hyperintensities from fluid-attenuated inversion recovery MRI, had normal cognition at the time of their MRI, and were administered the National Alzheimer's Coordinating Center Uniform Data Set neuropsychological test battery within 1 year of study evaluation and had at least two post-MRI time points of clinical data. Neuropsychiatric status was assessed by the Geriatric Depression Scale-15 and Neuropsychiatric Inventory-Questionnaire. Clinical Dementia Rating Sum of Boxes defined functional status. For participants subsequently diagnosed with mild cognitive impairment (MCI) or dementia, their impairment must have been attributed to Alzheimer's disease (AD) to evaluate the relationships between WMH and the clinical presentation of AD. Results: Of the 465 participants, 56 converted to MCI or AD dementia (average follow-up = 5 years). Among the 465 participants, generalized estimating equations controlling for age, sex, race, education, APOE ε4, and total brain and hippocampal volume showed that higher baseline log-white matter hyperintensities predicted accelerated decline on the following neuropsychological tests in rank order of effect size: Trails B (p < 0.01), Digit Symbol Coding (p < 0.01), Logical Memory Immediate Recall (p = 0.02), Trail Making A (p < 0.01), and Semantic Fluency (p < 0.01). White matter hyperintensities predicted increases in Clinical Dementia Rating Sum of Boxes (p < 0.01) and Geriatric Depression Scale-15 scores (p = 0.01). Effect sizes were comparable to total brain and hippocampal volume. White matter hyperintensities did not predict diagnostic conversion. All effects also remained after including individuals with non-AD suspected etiologies for those who converted to MCI or dementia. Conclusions: In this baseline cognitively normal sample, greater white matter hyperintensities were associated with accelerated cognitive, neuropsychiatric, and functional decline independent of traditional risk factors and MRI biomarkers for Alzheimer's disease. [ABSTRACT FROM AUTHOR]
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- 2019
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19. Higher BMI is associated with reduced brain volume in heart failure.
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Alosco ML, Brickman AM, Spitznagel MB, Narkhede A, Griffith EY, Raz N, Cohen R, Sweet LH, Colbert LH, Josephson R, Hughes J, Rosneck J, and Gunstad J
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Background: Heart failure (HF) patients are at risk for structural brain changes due to cerebral hypoperfusion. Past work shows obesity is linked with reduced cerebral blood flow and associated with brain atrophy in healthy individuals, although its effects on the brain in HF are unclear. This study examined the association among body mass index (BMI), cerebral perfusion, and brain volume in HF patients., Results: Eighty HF patients underwent transcranial Doppler sonography to quantify cerebral blood flow velocity of the middle cerebral artery (CBF-V of the MCA) and brain magnetic resonance imaging (MRI) to quantify total brain, total and subcortical gray matter, white matter volume, and white matter hyperintensities. Body mass index (BMI) operationalized weight status. Nearly 45% of HF patients exhibited a BMI consistent with obesity. Regression analyses adjusting for medical variables, demographic characteristics, and CBF-V of the MCA, showed increased BMI was associated with reduced white matter volume ( p <.05). BMI also interacted with cerebral perfusion to impact total gray matter volume, but this pattern did not emerge for any other MRI indices ( p < 0.05)., Conclusions: Our findings suggest increased BMI negatively affects brain volume in HF, and higher BMI interacts with cerebral perfusion to impact gray matter volume. The mechanisms for these findings remain unclear and likely involve multiple physiological processes. Prospective studies are needed to elucidate the exact pattern and rates of brain changes in obese HF persons.
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- 2014
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