This database contains 74 studies, archived under the term: "pathology"
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Docosahexaenoic acid supplementation and cognitive decline in Alzheimer disease: a randomized trial
Quinn, Joseph F.,
Raman, Rema,
Thomas, Ronald G.,
Yurko-Mauro, Karin,
Nelson, Edward B.,
van Dyck, Christopher,
Galvin, James E.,
Emond, Jennifer,
Jack, Clifford R., Jr.,
Weiner, Michael,
Shinto, Lynne,
Aisen, Paul S
Context: Docosahexaenoic acid (DHA) is the most abundant long-chain polyunsaturated fatty acid in the brain. Epidemiological studies suggest that consumption of DHA is associated with a reduced incidence of Alzheimer disease. Animal studies demonstrate that oral intake of DHA reduces Alzheimer-like brain pathology.; Objective: To determine if supplementation with DHA slows cognitive and functional decline […]
Increased glutamate in the hippocampus after galantamine treatment for Alzheimer disease
Penner, Jacob,
Rupsingh, Raul,
Smith, Matthew,
Wells, Jennie L.,
Borrie, Michael J.,
Bartha, Robert
Galantamine is a cholinesterase inhibitor and allosteric potentiating ligand modulating presynaptic nicotinic acetylcholine receptors that is used in the treatment of Alzheimer disease (AD). The purpose of this study was to determine if galantamine treatment would result in detectable hippocampal metabolite changes that correlated with changes in cognition, as measured by the Mini-Mental State Examination […]
Postmenopausal hormone therapy and subclinical cerebrovascular disease: the WHIMS-MRI Study
Coker, L. H.,
Hogan, P. E.,
Bryan, N. R.,
Kuller, L. H.,
Margolis, K. L.,
Bettermann, K.,
Wallace, R. B.,
Lao, Z.,
Freeman, R.,
Stefanick, M. L.,
Shumaker, S. A.
Objective: The Women’s Health Initiative Memory Study (WHIMS) hormone therapy (HT) trials reported that conjugated equine estrogen (CEE) with or without medroxyprogesterone acetate (MPA) increases risk for all-cause dementia and global cognitive decline. WHIMS MRI measured subclinical cerebrovascular disease as a possible mechanism to explain cognitive decline reported in WHIMS.; Methods: We contacted 2,345 women […]
Ibuprofen treatment modifies cortical sources of EEG rhythms in mild Alzheimer’s disease
Babiloni, Claudio,
Frisoni, Giovanni B.,
Del Percio, Claudio,
Zanetti, Orazio,
Bonomini, Cristina,
Cassetta, Emanuele,
Pasqualetti, Patrizio,
Miniussi, Carlo,
De Rosas, Mario,
Valenzano, Anna,
Cibelli, Giuseppe,
Eusebi, Fabrizio,
Rossini, Paolo M.
Objective: Non-steroidal anti-inflammatory drugs such as ibuprofen have a protective role on risk of Alzheimer’s disease (AD). Here we evaluated the hypothesis that long-term ibuprofen treatment affects cortical sources of resting electroencephalographic (EEG) rhythms in mild AD patients.; Methods: Twenty-three AD patients (13 treated AD IBUPROFEN; 10 untreated AD PLACEBO) were enrolled. Resting EEG data […]
Effects of aerobic exercise on mild cognitive impairment: a controlled trial
Baker, Laura D.,
Frank, Laura L.,
Foster-Schubert, Karen,
Green, Pattie S.,
Wilkinson, Charles W.,
McTiernan, Anne,
Plymate, Stephen R.,
Fishel, Mark A.,
Watson, G. Stennis,
Cholerton, Brenna A.,
Duncan, Glen E.,
Mehta, Pankaj D.,
Craft, Suzanne
Objectives: To examine the effects of aerobic exercise on cognition and other biomarkers associated with Alzheimer disease pathology for older adults with mild cognitive impairment, and assess the role of sex as a predictor of response.; Design: Six-month, randomized, controlled, clinical trial.; Setting: Veterans Affairs Puget Sound Health Care System clinical research unit.; Participants: Thirty-three […]
A phase I trial of deep brain stimulation of memory circuits in Alzheimer’s disease
Laxton, Adrian W.,
Tang-Wai, David F.,
McAndrews, Mary Pat,
Zumsteg, Dominik,
Wennberg, Richard,
Keren, Ron,
Wherrett, John,
Naglie, Gary,
Hamani, Clement,
Smith, Gwenn S.,
Lozano, Andres M.
Objective: Alzheimer disease (AD) is characterized by functional impairment in the neural elements and circuits underlying cognitive and memory functions. We hypothesized that fornix/hypothalamus deep brain stimulation (DBS) could modulate neurophysiological activity in these pathological circuits and possibly produce clinical benefits.; Methods: We conducted a phase I trial in 6 patients with mild AD receiving […]
Randomized controlled trial of atorvastatin in mild to moderate Alzheimer disease: LEADe
Feldman, H. H.,
Doody, R. S.,
Kivipelto, M.,
Sparks, D. L.,
Waters, D. D.,
Jones, R. W.,
Schwam, E.,
Schindler, R.,
Hey-Hadavi, J.,
DeMicco, D. A.,
Breazna, A.
Background: There is some evidence that statins may have a protective and symptomatic benefit in Alzheimer disease (AD). The LEADe study is a randomized controlled trial (RCT) evaluating the efficacy and safety of atorvastatin in patients with mild to moderate AD.; Methods: This was an international, multicenter, double-blind, randomized, parallel-group study. Subjects had mild to […]
Longitudinal changes in white matter disease and cognition in the first year of the Alzheimer disease neuroimaging initiative
Carmichael, Owen,
Schwarz, Christopher,
Drucker, David,
Fletcher, Evan,
Harvey, Danielle,
Beckett, Laurel,
Jack, Clifford R., Jr.,
Weiner, Michael,
DeCarli, Charles
Objective: To evaluate relationships between magnetic resonance imaging (MRI)-based measures of white matter hyperintensities (WMHs), measured at baseline and longitudinally, and 1-year cognitive decline using a large convenience sample in a clinical trial design with a relatively mild profile of cardiovascular risk factors.; Design: Convenience sample in a clinical trial design.; Subjects: A total of […]
Reduction of aggregated Tau in neuronal processes but not in the cell bodies after Abeta42 immunisation in Alzheimer’s disease
Boche, Delphine,
Donald, Jane,
Love, Seth,
Harris, Scott,
Neal, James W.,
Holmes, Clive,
Nicoll, James A. R.
Alzheimer’s disease (AD) pathology is characterised by aggregation in the brain of amyloid-beta (Abeta) peptide and hyperphosphorylated tau (phospho-tau), although how these proteins interact in disease pathogenesis is unclear. Abeta immunisation results in removal of Abeta from the brain but cognitive decline continues to progress, possibly due to persistent phospho-tau. We quantified phospho-tau and Abeta42 […]