16 results on '"Dichgans, Martin"'
Search Results
2. Associations of genetically predicted IL-6 signaling with cardiovascular disease risk across population subgroups
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Georgakis, Marios K., Malik, Rainer, Richardson, Tom G., Howson, Joanna M. M., Anderson, Christopher D., Burgess, Stephen, Hovingh, G. Kees, Dichgans, Martin, and Gill, Dipender
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- 2022
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3. Higher levels of myelin are associated with higher resistance against tau pathology in Alzheimer’s disease
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Rubinski, Anna, Franzmeier, Nicolai, Dewenter, Anna, Luan, Ying, Smith, Ruben, Strandberg, Olof, Ossenkoppele, Rik, Dichgans, Martin, Hansson, Oskar, and Ewers, Michael
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- 2022
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4. Proteomic profiling in cerebral amyloid angiopathy reveals an overlap with CADASIL highlighting accumulation of HTRA1 and its substrates
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Zellner, Andreas, Müller, Stephan A., Lindner, Barbara, Beaufort, Nathalie, Rozemuller, Annemieke J. M., Arzberger, Thomas, Gassen, Nils C., Lichtenthaler, Stefan F., Kuster, Bernhard, Haffner, Christof, and Dichgans, Martin
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- 2022
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5. PRediction of acute coronary syndrome in acute ischemic StrokE (PRAISE) – protocol of a prospective, multicenter trial with central reading and predefined endpoints
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Nolte, Christian H., von Rennenberg, Regina, Litmeier, Simon, Scheitz, Jan F., Leistner, David M., Blankenberg, Stephan, Dichgans, Martin, Katus, Hugo, Petzold, Gabor C., Pieske, Burkert, Regitz-Zagrosek, Vera, Wegscheider, Karl, Zeiher, Andreas M., Landmesser, Ulf, and Endres, Matthias
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- 2020
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6. The left frontal cortex supports reserve in aging by enhancing functional network efficiency
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Franzmeier, Nicolai, Hartmann, Julia, Taylor, Alexander N. W., Araque-Caballero, Miguel Á., Simon-Vermot, Lee, Kambeitz-Ilankovic, Lana, Bürger, Katharina, Catak, Cihan, Janowitz, Daniel, Müller, Claudia, Ertl-Wagner, Birgit, Stahl, Robert, Dichgans, Martin, Duering, Marco, and Ewers, Michael
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- 2018
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7. Higher CSF sTREM2 attenuates ApoE4-related risk for cognitive decline and neurodegeneration
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Franzmeier, Nicolai, Suárez-Calvet, M., Kleinberger, Gernot, Doraiswamy, P Murali, Petrella, Jeffrey R, Arnold, Steven E, Karlawish, Jason H, Wolk, David, Smith, Charles D, Jicha, Greg, Hardy, Peter, Lopez, Oscar L, Oakley, Mary Ann, Haass, Christian, Simpson, Donna M, Ismail, M Saleem, Brand, Connie, Mulnard, Ruth A, Thai, Gaby, Mc-Adams-Ortiz, Catherine, Diaz-Arrastia, Ramon, Martin-Cook, Kristen, DeVous, Michael, Levey, Allan I, Ewers, Michael, Lah, James J, Cellar, Janet S, Burns, Jeffrey M, Anderson, Heather S, Swerdlow, Russell H, Bartzokis, George, Silverman, Daniel H S, Lu, Po H, Apostolova, Liana, Graff-Radford, Neill R, Initiative, Alzheimer’s Disease Neuroimaging, Parfitt, Francine, Johnson, Heather, Farlow, Martin, Herring, Scott, Hake, Ann M, van Dyck, Christopher H, Carson, Richard E, MacAvoy, Martha G, Chertkow, Howard, Bergman, Howard, Weiner, Michael, Hosein, Chris, Black, Sandra, Stefanovic, Bojana, Caldwell, Curtis, Hsiung, Ging-Yuek Robin, Feldman, Howard, Assaly, Michele, Kertesz, Andrew, Rogers, John, Trost, Dick, Aisen, Paul, Bernick, Charles, Munic, Donna, Wu, Chuang-Kuo, Johnson, Nancy, Mesulam, Marsel, Sadowsky, Carl, Martinez, Walter, Villena, Teresa, Turner, Raymond Scott, Johnson, Kathleen, Novak, Gerald, Reynolds, Brigid, Sperling, Reisa A, Frey, Meghan, Johnson, Keith A, Rosen, Allyson, Tinklenberg, Jared, Ashford, Wes, Sabbagh, Marwan, Belden, Christine, Jacobson, Sandra, Green, Robert C, Killiany, Ronald, Norbash, Alexander, Nair, Anil, Obisesan, Thomas O, Wolday, Saba, Bwayo, Salome K, Lerner, Alan, Hudson, Leon, Ogrocki, Paula, Fletcher, Evan, Montine, Tom, Carmichael, Owen, Kittur, Smita, Borrie, Michael, Lee, T-Y, Bartha, Rob, Johnson, Sterling, Asthana, Sanjay, Carlsson, Cynthia M, Potkin, Steven G, Preda, Adrian, Petersen, Ronald, Nguyen, Dana, Tariot, Pierre, Fleisher, Adam, Reeder, Stephanie, Bates, Vernice, Capote, Horacio, Rainka, Michelle, Hendin, Barry A, Scharre, Douglas W, Kataki, Maria, Frontzkowski, Lukas, Gamst, Anthony, Zimmerman, Earl A, Celmins, Dzintra, Brown, Alice D, Hosp, Hartford, Pearlson, Godfrey D, Blank, Karen, Anderson, Karen, Santulli, Robert B, Schwartz, Eben S, Williamson, Jeff D, Thomas, Ronald G, Sink, Kaycee M, Watkins, Franklin, Ott, Brian R, Querfurth, Henry, Tremont, Geoffrey, Salloway, Stephen, Malloy, Paul, Correia, Stephen, Rosen, Howard J, Miller, Bruce L, Donohue, Michael, Mintzer, Jacobo, Longmire, Crystal Flynn, Spicer, Kenneth, Walter, Sarah, Gessert, Devon, Sather, Tamie, Beckett, Laurel, Harvey, Danielle, Kornak, John, Jack, Clifford R, Moore, Annah, Dale, Anders, Bernstein, Matthew, Felmlee, Joel, Fox, Nick, Thompson, Paul, Schuff, Norbert, Alexander, Gene, DeCarli, Charles, Jagust, William, Bandy, Dan, Hohman, Timothy J, Koeppe, Robert A, Foster, Norm, Reiman, Eric M, Chen, Kewei, Mathis, Chet, Morris, John, Cairns, Nigel J, Taylor-Reinwald, Lisa, Trojanowki, J. Q., Shaw, Les, Morenas-Rodriguez, Estrella, Lee, Virginia M Y, Korecka, Magdalena, Toga, Arthur W, Crawford, Karen, Neu, Scott, Saykin, Andrew J, Foroud, Tatiana M, Potkin, Steven, Shen, Li, Kachaturian, Zaven, Nuscher, Brigitte, Frank, Richard, Snyder, Peter J, Molchan, Susan, Kaye, Jeffrey, Dolen, Sara, Quinn, Joseph, Schneider, Lon S, Pawluczyk, Sonia, Spann, Bryan M, Brewer, James, Shaw, Leslie, Vanderswag, Helen, Heidebrink, Judith L, Lord, Joanne L, Johnson, Kris, Doody, Rachelle S, Villanueva-Meyer, Javier, Chowdhury, Munir, Stern, Yaakov, Honig, Lawrence S, Bell, Karen L, Trojanowski, John Q, Morris, John C, Mintun, Mark A, Schneider, Stacy, Marson, Daniel, Griffith, Randall, Clark, David, Grossman, Hillel, Mitsis, Effie, Romirowsky, Aliza, deToledo-Morrell, Leyla, Dichgans, Martin, Shah, Raj C, Duara, Ranjan, Varon, Daniel, Roberts, Peggy, Albert, Marilyn, Onyike, Chiadi, Kielb, Stephanie, Rusinek, Henry, de Leon, Mony J, and Glodzik, Lidia
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Male ,Aging ,pathology [Cognitive Dysfunction] ,Apolipoprotein E4 ,Cognitive decline ,genetics [Alzheimer Disease] ,Neurodegenerative ,lcsh:Geriatrics ,Alzheimer's Disease ,lcsh:RC346-429 ,pathology [Alzheimer Disease] ,Immunologic ,Receptors ,80 and over ,2.1 Biological and endogenous factors ,sTREM2 ,Microglial activation ,Aetiology ,Receptors, Immunologic ,genetics [Apolipoprotein E4] ,Aged, 80 and over ,Membrane Glycoproteins ,pathology [Nerve Degeneration] ,cerebrospinal fluid [Alzheimer Disease] ,cerebrospinal fluid [Cognitive Dysfunction] ,Neurological ,Female ,cerebrospinal fluid [Membrane Glycoproteins] ,Alzheimer’s disease ,Research Article ,Clinical Sciences ,ApoE4 ,Clinical Research ,Alzheimer Disease ,ddc:570 ,Acquired Cognitive Impairment ,Genetics ,Humans ,Cognitive Dysfunction ,Genetic Predisposition to Disease ,Neurodegeneration ,lcsh:Neurology. Diseases of the nervous system ,Aged ,Neurology & Neurosurgery ,Neurosciences ,genetics [Cognitive Dysfunction] ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Alzheimer’s Disease Neuroimaging Initiative ,Brain Disorders ,lcsh:RC952-954.6 ,Nerve Degeneration ,Dementia - Abstract
Background The Apolipoprotein E ε4 allele (i.e. ApoE4) is the strongest genetic risk factor for sporadic Alzheimer’s disease (AD). TREM2 (i.e. Triggering receptor expressed on myeloid cells 2) is a microglial transmembrane protein brain that plays a central role in microglia activation in response to AD brain pathologies. Whether higher TREM2-related microglia activity modulates the risk to develop clinical AD is an open question. Thus, the aim of the current study was to assess whether higher sTREM2 attenuates the effects of ApoE4-effects on future cognitive decline and neurodegeneration. Methods We included 708 subjects ranging from cognitively normal (CN, n = 221) to mild cognitive impairment (MCI, n = 414) and AD dementia (n = 73) from the Alzheimer’s disease Neuroimaging Initiative. We used linear regression to test the interaction between ApoE4-carriage by CSF-assessed sTREM2 levels as a predictor of longitudinally assessed cognitive decline and MRI-assessed changes in hippocampal volume changes (mean follow-up of 4 years, range of 1.7-7 years). Results Across the entire sample, we found that higher CSF sTREM2 at baseline was associated with attenuated effects of ApoE4-carriage (i.e. sTREM2 x ApoE4 interaction) on longitudinal global cognitive (p = 0.001, Cohen’s f 2 = 0.137) and memory decline (p = 0.006, Cohen’s f 2 = 0.104) as well as longitudinally assessed hippocampal atrophy (p = 0.046, Cohen’s f 2 = 0.089), independent of CSF markers of primary AD pathology (i.e. Aβ1–42, p-tau181). While overall effects of sTREM2 were small, exploratory subanalyses stratified by diagnostic groups showed that beneficial effects of sTREM2 were pronounced in the MCI group. Conclusion Our results suggest that a higher CSF sTREM2 levels are associated with attenuated ApoE4-related risk for future cognitive decline and AD-typical neurodegeneration. These findings provide further evidence that TREM2 may be protective against the development of AD.
- Published
- 2020
8. Impact of the COVID-19-pandemic on thrombectomy services in Germany
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Tiedt, Steffen, Bode, Felix J, Bormann, Albrecht, Braun, Michael, Dichgans, Martin, Dorn, Franziska, Eckert, Bernd, Ernemann, Ulrike, Fiehler, Jens, Gerloff, Christian, Hamann, Gerhard F, Henn, Karl-Heinz, Uphaus, Timo, Keil, Fee, Kellert, Lars, Kraemer, Christoffer, Liman, Jan, Ludolph, Alexander, Nolte, Christan H, Petersen, Martina, Pfeilschifter, Waltraud, Poli, Sven, Röther, Joachim, Alegiani, Anna, Siebert, Eberhard, Siedow, Andreas, Solymosi, Laszlo, Stögbauer, Florian, Thomalla, Götz, Wunderlich, Silke, Zweynert, Sarah, Gröschel, Klaus, Petzold, Gabor Claus Julius Peter, investigators, GSR-ET, Berrouschot, Jörg, Boeckh-Behrens, Tobias, and Bohner, Georg
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medicine.medical_specialty ,Coronavirus disease 2019 (COVID-19) ,business.industry ,COVID-19 ,medicine.disease ,Large cohort ,Stroke ,Occlusion ,Emergency medicine ,Pandemic ,Medicine ,In patient ,Neurosurgery ,ddc:610 ,business ,Large vessel occlusion ,Research Article ,Neuroradiology ,Outcome ,Thrombectomy - Abstract
Background The Coronavirus Disease 2019 (COVID-19) pandemic may have altered emergency workflows established to optimize the outcome of patients with large-vessel occlusion (LVO) stroke. Aims We here analyzed workflow time intervals and functional outcomes of LVO patients treated with endovascular thrombectomy (ET) during the COVID-19 pandemic in Germany. Methods We compared the frequency, pre- and intrahospital workflow time intervals, rates of reperfusion, and functional outcome of patients admitted from March 1st to May 31st 2020 with patients admitted during the same time interval in 2019 to 12 university and municipal hospitals across Germany (N = 795). Results The number of LVO patients treated with ET between March to May 2020 was similar when compared to the same interval in 2019. Direct-to-center patients and patients admitted through interhospital transfer in 2020 showed similar pre- and intrahospital workflow time intervals compared to patients admitted in 2019, except for a longer door-to-groin time in patients admitted through interhospital transfer in 2020 (47 min vs 38 min, p = 0.005). Rates of reperfusion were not significantly different between 2020 and 2019. Functional outcome at discharge of LVO patients treated in 2020 was not significantly different compared to patients treated in 2019. Conclusion Pre- and intrahospital workflows, ET efficacy, and functional outcome of LVO patients treated with ET were not affected during the COVID-19 pandemic in our large cohort from centers across Germany.
- Published
- 2020
9. Tau-PET and in vivo Braak-staging as prognostic markers of future cognitive decline in cognitively normal to demented individuals.
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Biel, Davina, Brendel, Matthias, Rubinski, Anna, Buerger, Katharina, Janowitz, Daniel, Dichgans, Martin, and Franzmeier, Nicolai
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PROGNOSIS ,OLDER people ,COGNITION disorders ,MILD cognitive impairment ,DEMENTIA ,EPISODIC memory ,COGNITION - Abstract
Background: To systematically examine the clinical utility of tau-PET and Braak-staging as prognostic markers of future cognitive decline in older adults with and without cognitive impairment. Methods: In this longitudinal study, we included 396 cognitively normal to dementia subjects with
18 F-Florbetapir/18 F-Florbetaben-amyloid-PET,18 F-Flortaucipir-tau-PET and ~ 2-year cognitive follow-up. Annual change rates in global cognition (i.e., MMSE, ADAS13) and episodic memory were calculated via linear-mixed models. We determined global amyloid-PET (Centiloid) plus global and Braak-stage-specific tau-PET SUVRs, which were stratified as positive(+ )/negative(− ) at pre-established cut-offs, classifying subjects as Braak0 /BraakI+ /BraakI–IV+ /BraakI–VI+ /Braakatypical+ . In bootstrapped linear regression, we assessed the predictive accuracy of global tau-PET SUVRs vs. Centiloid on subsequent cognitive decline. To test for independent tau vs. amyloid effects, analyses were further controlled for the contrary PET-tracer. Using ANCOVAs, we tested whether more advanced Braak-stage predicted accelerated future cognitive decline. All models were controlled for age, sex, education, diagnosis, and baseline cognition. Lastly, we determined Braak-stage-specific conversion risk to mild cognitive impairment (MCI) or dementia. Results: Baseline global tau-PET SUVRs explained more variance (partial R2 ) in future cognitive decline than Centiloid across all cognitive tests (Cohen's d ~ 2, all tests p < 0.001) and diagnostic groups. Associations between tau-PET and cognitive decline remained consistent when controlling for Centiloid, while associations between amyloid-PET and cognitive decline were non-significant when controlling for tau-PET. More advanced Braak-stage was associated with gradually worsening future cognitive decline, independent of Centiloid or diagnostic group (p < 0.001), and elevated conversion risk to MCI/dementia. Conclusion: Tau-PET and Braak-staging are highly predictive markers of future cognitive decline and may be promising single-modality estimates for prognostication of patient-specific progression risk in clinical settings. [ABSTRACT FROM AUTHOR]- Published
- 2021
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10. Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) as a model of small vessel disease: update on clinical, diagnostic, and management aspects.
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Di Donato, Ilaria, Bianchi, Silvia, De Stefano, Nicola, Dichgans, Martin, Dotti, Maria Teresa, Duering, Marco, Jouvent, Eric, Korczyn, Amos D., Lesnik-Oberstein, Saskia A. J., Malandrini, Alessandro, Markus, Hugh S., Pantoni, Leonardo, Penco, Silvana, Rufa, Alessandra, Sinanović, Osman, Stojanov, Dragan, and Federico, Antonio
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CADASIL syndrome ,NEUROLOGICAL disorders ,BRAIN imaging ,MONOGENIC & polygenic inheritance (Genetics) ,GENETIC disorders ,DIAGNOSIS ,CEREBRAL small vessel diseases ,DISEASE complications - Abstract
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the most common and best known monogenic small vessel disease. Here, we review the clinical, neuroimaging, neuropathological, genetic, and therapeutic aspects based on the most relevant articles published between 1994 and 2016 and on the personal experience of the authors, all directly involved in CADASIL research and care. We conclude with some suggestions that may help in the clinical practice and management of these patients. [ABSTRACT FROM AUTHOR]
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- 2017
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11. The carotid plaque imaging in acute stroke (CAPIAS) study: protocol and initial baseline data
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Bayer-Karpinska, Anna, Schwarz, Florian, Wollenweber, Frank A, Poppert, Holger, Boeckh-Behrens, Tobias, Becker, Alexander, Clevert, Dirk A, Nikolaou, Konstantin, Opherk, Christian, Dichgans, Martin, and Saam, Tobias
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Male ,Time Factors ,Clinical Neurology ,Observation ,Cryptogenic stroke ,Plaque imaging ,Neuropsychological Tests ,Functional Laterality ,Cohort Studies ,Study Protocol ,Germany ,Outcome Assessment, Health Care ,Image Processing, Computer-Assisted ,Humans ,Carotid Stenosis ,cardiovascular diseases ,Aged ,Cerebral Cortex ,Interleukins ,Middle Aged ,Atherosclerosis ,Creatine ,Stroke ,Echocardiography ,Disease Progression ,Female ,Internal carotid artery ,Cognition Disorders ,MRI - Abstract
Background In up to 30% of patients with ischemic stroke no definite etiology can be established. A significant proportion of cryptogenic stroke cases may be due to non-stenosing atherosclerotic plaques or low grade carotid artery stenosis not fulfilling common criteria for atherothrombotic stroke. The aim of the CAPIAS study is to determine the frequency, characteristics, clinical and radiological long-term consequences of ipsilateral complicated American Heart Association lesion type VI (AHA-LT VI) carotid artery plaques in patients with cryptogenic stroke. Methods/Design 300 patients (age >49 years) with unilateral DWI-positive lesions in the anterior circulation and non- or moderately stenosing (
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- 2013
12. Comparison of symptomatic and asymptomatic atherosclerotic carotid plaques using parallel imaging and 3 T black-blood in vivo CMR.
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Grimm, Jochen M., Schindler, Andreas, Freilinger, Tobias, Cyran, Clemens C., Bamberg, Fabian, Chun Yuan, Reiser, Maximilian F., Dichgans, Martin, Freilinger, Caroline, Nikolaou, Konstantin, and Saam, Tobias
- Abstract
Background: To determine if black-blood 3 T cardiovascular magnetic resonance (bb-CMR) can depict differences between symptomatic and asymptomatic carotid atherosclerotic plaques in acute ischemic stroke patients. Methods: In this prospective monocentric observational study 34 patients (24 males; 70 ±9.3 years) with symptomatic carotid disease defined as ischemic brain lesions in one internal carotid artery territory on diffusion weighted images underwent a carotid bb-CMR at 3 T with fat-saturated pre- and post-contrast T1w-, PDw-, T2w- and TOF images using surface coils and Parallel Imaging techniques (PAT factor = 2) within 10 days after symptom onset. All patients underwent extensive clinical workup (lab, brain MR, duplex sonography, 24-hour ECG, transesophageal echocardiography) to exclude other causes of ischemic stroke. Prevalence of American Heart Association lesion type VI (AHA-LT6), status of the fibrous cap, presence of hemorrhage/thrombus and area measurements of calcification, necrotic core and hemorrhage were determined in both carotid arteries in consensus by two reviewers who were blinded to clinical information. McNemar and Wilcoxon's signed rank tests were use for statistical comparison. A p-value <0.05 was considered statistically significant. Results: Symptomatic plaques showed a higher prevalence of AHA-LT6 (67.7% vs. 11.8%; p < 0.001; odds ratio = 12.5), ruptured fibrous caps (44.1% vs. 2.9%; p < 0.001; odds ratio = 15.0), juxtaluminal thrombus (26.5 vs. 0%; p < 0.01; odds ratio = 7.3) and intraplaque hemorrhage (58.6% vs. 11.8%; p = 0.01; odds ratio = 3.8). Necrotic core and hemorrhage areas were greater in symptomatic plaques (14.1 mm2 vs. 5.5 mm2 and 13.6 mm2 vs. 5.3 mm2; p < 0.01, respectively). Conclusion: 3 T bb-CMR is able to differentiate between symptomatic and asymptomatic carotid plaques, demonstrating the potential of bb-CMR to differentiate between stable and vulnerable lesions and ultimately to identify patients with low versus high risk for cardiovascular complications. Best predictors of the symptomatic side were a ruptured fibrous cap, AHA-LT 6, juxtaluminal hemorrhage/thrombus, and intraplaque hemorrhage. [ABSTRACT FROM AUTHOR]
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- 2013
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13. Characteristics of carotid atherosclerotic plaques of chronic lipid apheresis patients as assessed by In Vivo High-Resolution CMR - a comparative analysis.
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Grimm, Jochen M., Nikolaou, Konstantin, Schindler, Andreas, Hettich, Reinhard, Heigl, Franz, Cyran, Clemens C., Schwarz, Florian, Klingel, Reinhard, Karpinska, Anna, Chun Yuan, Dichgans, Martin, Reiser, Maximilian F., and Saam, Tobias
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LIPIDS , *CORONARY disease , *CARDIOVASCULAR diseases risk factors , *BIOMOLECULES , *HEART diseases , *ARTERIOSCLEROSIS risk factors , *LIPID analysis , *AGE distribution , *CAROTID artery diseases , *COMPARATIVE studies , *FISHER exact test , *HEMAPHERESIS , *HYPERCHOLESTEREMIA , *MAGNETIC resonance imaging , *PROBABILITY theory , *STROKE , *T-test (Statistics) , *FAMILY history (Medicine) , *DESCRIPTIVE statistics , *DISEASE risk factors ,CAROTID artery stenosis - Abstract
Background: Components of carotid atherosclerotic plaques can reliably be identified and quantified using high resolution in vivo 3-Tesla CMR. It is suspected that lipid apheresis therapy in addition to lowering serum lipid levels also has an influence on development and progression of atherosclerotic plaques. The purpose of this study was to evaluate the influence of chronic lipid apheresis (LA) on the composition of atherosclerotic carotid plaques. Methods: 32 arteries of 16 patients during chronic LA-therapy with carotid plaques and stenosis of 1-80% were matched according to degree of stenosis with 32 patients, who had recently suffered an ischemic stroke. Of these patients only the asymptomatic carotid artery was analyzed. All patients underwent black-blood 3 T CMR of the carotids using parallel imaging and dedicated surface coils. Cardiovascular risk factors were recorded. Morphology and composition of carotid plaques were evaluated. For statistical evaluation Fisher's Exact and unpaired t-test were used. A p-value <0.05 was considered statistically significant. Results: Patients in the LA-group were younger (63.5 vs. 73.9. years, p<0.05), had a higher prevalence of hypercholesterolemia and of established coronary heart disease in patients and in first-degree relatives (p<0.05, respectively). LA-patients had smaller maximum wall areas (49.7 vs. 59.6mm2, p<0.05), showed lower prevalence of lipid cores (28.1% vs. 56.3%, p<0.05) and the lipid content was smaller than in the control group (5.0 vs. 11.6%, p<0.05). Minimum lumen areas and maximum total vessel areas did not differ significantly between both groups. Conclusion: Results of this study suggest that, despite a severer risk profile for cardiovascular complications in LA-patients, chronic LA is associated with significantly lower lipid content in carotid plaques compared to plaques of patients without LA with similar degrees of stenosis, which is characteristic of clinically stable plaques. [ABSTRACT FROM AUTHOR]
- Published
- 2012
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14. Prevalence of complicated carotid atherosclerotic plaques ispilateral to ischemic cryptogenic stroke using high-resolution mri.
- Author
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Saam, Tobias, Freilinger, Tobias, Schindler, Andreas, Grimm, Jochen, Schmidt, Caroline, Bamberg, Fabian, Dichgans, Martin, Chun Yuan, Reiser, Maximilian F., and Nikolaou, Konstantin
- Subjects
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ATHEROSCLEROTIC plaque - Abstract
An abstract of the paper "Prevalence of complicated carotid atherosclerotic plaques ispilateral to ischemic cryptogenic stroke using high-resolution mri," by Tobias Saam, and colleagues from the 2011 SCMR/Euro CMR Joint Scientific Sessions in Nice, France from February 3-6, 2011 is presented.
- Published
- 2011
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15. Higher CSF sTREM2 attenuates ApoE4-related risk for cognitive decline and neurodegeneration.
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Franzmeier N, Suárez-Calvet M, Frontzkowski L, Moore A, Hohman TJ, Morenas-Rodriguez E, Nuscher B, Shaw L, Trojanowski JQ, Dichgans M, Kleinberger G, Haass C, and Ewers M
- Subjects
- Aged, Aged, 80 and over, Alzheimer Disease pathology, Apolipoprotein E4 genetics, Cognitive Dysfunction pathology, Female, Genetic Predisposition to Disease, Humans, Male, Nerve Degeneration pathology, Receptors, Immunologic, Alzheimer Disease cerebrospinal fluid, Alzheimer Disease genetics, Cognitive Dysfunction cerebrospinal fluid, Cognitive Dysfunction genetics, Membrane Glycoproteins cerebrospinal fluid
- Abstract
Background: The Apolipoprotein E ε4 allele (i.e. ApoE4) is the strongest genetic risk factor for sporadic Alzheimer's disease (AD). TREM2 (i.e. Triggering receptor expressed on myeloid cells 2) is a microglial transmembrane protein brain that plays a central role in microglia activation in response to AD brain pathologies. Whether higher TREM2-related microglia activity modulates the risk to develop clinical AD is an open question. Thus, the aim of the current study was to assess whether higher sTREM2 attenuates the effects of ApoE4-effects on future cognitive decline and neurodegeneration., Methods: We included 708 subjects ranging from cognitively normal (CN, n = 221) to mild cognitive impairment (MCI, n = 414) and AD dementia (n = 73) from the Alzheimer's disease Neuroimaging Initiative. We used linear regression to test the interaction between ApoE4-carriage by CSF-assessed sTREM2 levels as a predictor of longitudinally assessed cognitive decline and MRI-assessed changes in hippocampal volume changes (mean follow-up of 4 years, range of 1.7-7 years)., Results: Across the entire sample, we found that higher CSF sTREM2 at baseline was associated with attenuated effects of ApoE4-carriage (i.e. sTREM2 x ApoE4 interaction) on longitudinal global cognitive (p = 0.001, Cohen's f
2 = 0.137) and memory decline (p = 0.006, Cohen's f2 = 0.104) as well as longitudinally assessed hippocampal atrophy (p = 0.046, Cohen's f2 = 0.089), independent of CSF markers of primary AD pathology (i.e. Aβ1-42 , p-tau181 ). While overall effects of sTREM2 were small, exploratory subanalyses stratified by diagnostic groups showed that beneficial effects of sTREM2 were pronounced in the MCI group., Conclusion: Our results suggest that a higher CSF sTREM2 levels are associated with attenuated ApoE4-related risk for future cognitive decline and AD-typical neurodegeneration. These findings provide further evidence that TREM2 may be protective against the development of AD.- Published
- 2020
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16. Sequestration of latent TGF-β binding protein 1 into CADASIL-related Notch3-ECD deposits.
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Kast J, Hanecker P, Beaufort N, Giese A, Joutel A, Dichgans M, Opherk C, and Haffner C
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- CADASIL metabolism, Case-Control Studies, Female, HEK293 Cells, Humans, Male, Mutation genetics, Protein Structure, Tertiary, Receptor, Notch3, Receptors, Notch genetics, Sequence Analysis, Protein, Silver Staining, Statistics, Nonparametric, Transfection, Brain metabolism, CADASIL pathology, Latent TGF-beta Binding Proteins metabolism, Receptors, Notch metabolism
- Abstract
Introduction: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) represents the most common hereditary form of cerebral small vessel disease characterized by early-onset stroke and premature dementia. It is caused by mutations in the transmembrane receptor Notch3, which promote the aggregation and accumulation of the Notch3 extracellular domain (Notch3-ECD) within blood vessel walls. This process is believed to mediate the abnormal recruitment and dysregulation of additional factors including extracellular matrix (ECM) proteins resulting in brain vessel dysfunction. Based on recent evidence indicating a role for the transforming growth factor-β (TGF-β) pathway in sporadic and familial small vessel disease we studied fibronectin, fibrillin-1 and latent TGF-β binding protein 1 (LTBP-1), three ECM constituents involved in the regulation of TGF-β bioavailability, in post-mortem brain tissue from CADASIL patients and control subjects., Results: Fibronectin and fibrillin-1 were found to be enriched in CADASIL vessels without co-localizing with Notch3-ECD deposits, likely as a result of fibrotic processes secondary to aggregate formation. In contrast, LTBP-1 showed both an accumulation and a striking co-localization with Notch3-ECD deposits suggesting specific recruitment into aggregates. We also detected increased levels of the TGF-β prodomain (also known as latency-associated peptide, LAP) indicating dysregulation of the TGF-β pathway in CADASIL development. In vitro analyses revealed a direct interaction between LTBP-1 and Notch3-ECD and demonstrated a specific co-aggregation of LTBP-1 with mutant Notch3., Conclusion: We propose LTBP-1 as a novel component of Notch3-ECD deposits and suggest its involvement in pathological processes triggered by Notch3-ECD aggregation.
- Published
- 2014
- Full Text
- View/download PDF
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