@incollection{LanzlSeidovaDuehringetal.2009,
  author    = {Lanzl, I. and Seidova, S.-F. and D{\"u}hring, C. von and Kotliar, Konstantin},
  title     = {Befunde der dynamischen Gef{\"a}ßanalyse am Auge bei Gesunden und Glaukom-Patienten mit praxisrelevanter Bedeutung},
  series = {Mikrozirkulation beim Glaukom},
  booktitle = {Mikrozirkulation beim Glaukom},
  editor    = {Erb, Carl},
  publisher = {Elsevier},
  address   = {Amsterdam},
  pages     = {33 -- 39},
  year      = {2009},
  language  = {de}
}
@article{HanssenNickelDrexeletal.2011,
  author    = {Hanssen, H. and Nickel, T. and Drexel, V. and Hertel, G. and Emslander, I. and Sisic, Z. and Lorang, D. and Schuster, T. and Kotliar, Konstantin and Pressler, A. and Schmidt-Trucks{\"a}ss, A. and Weis, M. and Halle, M.},
  title     = {Exercise-induced alterations of retinal vessel diameters and cardiovascular risk reduction in obesity},
  series = {Atherosclerosis},
  volume    = {216},
  journal   = {Atherosclerosis},
  number    = {2},
  publisher = {Elsevier},
  address   = {Amsterdam},
  isbn      = {0021-9150},
  pages     = {433 -- 439},
  year      = {2011},
  language  = {en}
}
@article{KotliarLanzlSchmidtTrucksaessetal.2011,
  author    = {Kotliar, Konstantin and Lanzl, Ines M. and Schmidt-Trucks{\"a}ss, A. and Sitnikova, Diana and Ali, Mohammad and Blume, Katharina and Halle, Martin and Hansser, Henner},
  title     = {Dynamic retinal vessel response to flicker in obesity: A methodological approach},
  series = {Microvascular Research},
  volume    = {81},
  journal   = {Microvascular Research},
  number    = {1},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0026-2862},
  pages     = {123 -- 128},
  year      = {2011},
  language  = {en}
}
@article{AlbannaLuekeSchubertetal.2019,
  author    = {Albanna, Walid and L{\"u}ke, Jan Niklas and Schubert, Gerrit Alexander and Dibu{\´e}-Adjei, Maxine and Kotliar, Konstantin and Hescheler, J{\"u}rgen and Clusmann, Hans and Steiger, Hans-Jakob and H{\"a}nggi, Daniel and Kamp, Marcel A. and Schneider, Toni and Neumaier, Felix},
  title     = {Modulation of Ca v 2.3 channels by unconjugated bilirubin (UCB) - Candidate mechanism for UCB-induced neuromodulation and neurotoxicity},
  series = {Molecular and Cellular Neuroscience},
  volume    = {96},
  journal   = {Molecular and Cellular Neuroscience},
  number    = {4},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {1044-7431},
  doi       = {10.1016/j.mcn.2019.03.003},
  pages     = {35 -- 46},
  year      = {2019},
  language  = {en}
}
@article{NeumaierWeissVeldemanetal.2021,
  author    = {Neumaier, Felix and Weiss, Miriam and Veldeman, Michael and Kotliar, Konstantin and Wiesmann, Martin and Schulze-Steinen, Henna and H{\"o}llig, Anke and Clusmann, Hans and Schubert, Gerrit Alexander and Albanna, Walid},
  title     = {Changes in endogenous daytime melatonin levels after aneurysmal subarachnoid hemorrhage - preliminary findings from an observational cohort study},
  series = {Clinical Neurology and Neurosurgery},
  volume    = {208},
  journal   = {Clinical Neurology and Neurosurgery},
  number    = {Article No.: 106870},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0303-8467},
  doi       = {10.1016/j.clineuro.2021.106870},
  year      = {2021},
  abstract  = {Aneurysmal subarachnoid hemorrhage (aSAH) is associated with early and delayed brain injury due to several underlying and interrelated processes, which include inflammation, oxidative stress, endothelial, and neuronal apoptosis. Treatment with melatonin, a cytoprotective neurohormone with anti-inflammatory, anti-oxidant and anti-apoptotic effects, has been shown to attenuate early brain injury (EBI) and to prevent delayed cerebral vasospasm in experimental aSAH models. Less is known about the role of endogenous melatonin for aSAH outcome and how its production is altered by the pathophysiological cascades initiated during EBI. In the present observational study, we analyzed changes in melatonin levels during the first three weeks after aSAH.},
  language  = {en}
}
@article{KotliarOrtnerConradietal.2022,
  author    = {Kotliar, Konstantin and Ortner, Marion and Conradi, Anna and Hacker, Patricia and Hauser, Christine and G{\"u}nthner, Roman and Moser, Michaela and Muggenthaler, Claudia and Diehl-Schmid, Janine and Priller, Josef and Schmaderer, Christoph and Grimmer, Timo},
  title     = {Altered retinal cerebral vessel oscillation frequencies in Alzheimer's disease compatible with impaired amyloid clearance},
  series = {Neurobiology of Aging},
  volume    = {120},
  journal   = {Neurobiology of Aging},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0197-4580},
  doi       = {10.1016/j.neurobiolaging.2022.08.012},
  pages     = {117 -- 127},
  year      = {2022},
  abstract  = {Retinal vessels are similar to cerebral vessels in their structure and function. Moderately low oscillation frequencies of around 0.1 Hz have been reported as the driving force for paravascular drainage in gray matter in mice and are known as the frequencies of lymphatic vessels in humans. We aimed to elucidate whether retinal vessel oscillations are altered in Alzheimer's disease (AD) at the stage of dementia or mild cognitive impairment (MCI). Seventeen patients with mild-to-moderate dementia due to AD (ADD); 23 patients with MCI due to AD, and 18 cognitively healthy controls (HC) were examined using Dynamic Retinal Vessel Analyzer. Oscillatory temporal changes of retinal vessel diameters were evaluated using mathematical signal analysis. Especially at moderately low frequencies around 0.1 Hz, arterial oscillations in ADD and MCI significantly prevailed over HC oscillations and correlated with disease severity. The pronounced retinal arterial vasomotion at moderately low frequencies in the ADD and MCI groups would be compatible with the view of a compensatory upregulation of paravascular drainage in AD and strengthen the amyloid clearance hypothesis.},
  language  = {en}
}
@article{SmithKotliarLammertynetal.2020,
  author    = {Smith, Wayne and Kotliar, Konstantin and Lammertyn, Leandi and Ramoshaba, Nthai E. and Vilser, Walthard and Huisman, Hugo W. and Schutte, Aletta E.},
  title     = {Retinal vessel caliber and caliber responses in true normotensive black and white adults: The African-PREDICT study},
  series = {Microvascular Research},
  volume    = {128},
  journal   = {Microvascular Research},
  number    = {Article 103937},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0026-2862},
  doi       = {10.1016/j.mvr.2019.103937},
  year      = {2020},
  abstract  = {Purpose Globally, a detrimental shift in cardiovascular disease risk factors and a higher mortality level are reported in some black populations. The retinal microvasculature provides early insight into the pathogenesis of systemic vascular diseases, but it is unclear whether retinal vessel calibers and acute retinal vessel functional responses differ between young healthy black and white adults. Methods We included 112 black and 143 white healthy normotensive adults (20-30 years). Retinal vessel calibers (central retinal artery and vein equivalent (CRAE and CRVE)) were calculated from retinal images and vessel caliber responses to flicker light induced provocation (FLIP) were determined. Additionally, ambulatory blood pressure (BP), anthropometry and blood samples were collected. Results The groups displayed similar 24 h BP profiles and anthropometry (all p > .24). Black participants demonstrated a smaller CRAE (158 ± 11 vs. 164 ± 11 MU, p < .001) compared to the white group, whereas CRVE was similar (p = .57). In response to FLIP, artery maximal dilation was greater in the black vs. white group (5.6 ± 2.1 vs. 3.3 ± 1.8\%; p < .001). Conclusions Already at a young age, healthy black adults showed narrower retinal arteries relative to the white population. Follow-up studies are underway to show if this will be related to increased risk for hypertension development. The reason for the larger vessel dilation responses to FLIP in the black population is unclear and warrants further investigation.},
  language  = {en}
}
@article{PresslerEsefeldScherretal.2010,
  author    = {Pressler, Axel and Esefeld, Katrin and Scherr, Johannes and Ali, Mohammad and Hanssen, Henner and Kotliar, Konstantin and Lanzl, Ines and Halle, Martin and Kaemmerer, Harald and Schmidt-Trucks{\"a}ss, Arno and Hager, Alfred},
  title     = {Structural alterations of retinal arterioles in adults late after repair of aortic isthmic coarctation},
  series = {The American Journal of Cardiology},
  volume    = {105},
  journal   = {The American Journal of Cardiology},
  number    = {5},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0002-9149},
  doi       = {10.1016/j.amjcard.2009.10.070},
  pages     = {740 -- 744},
  year      = {2010},
  abstract  = {Patients after coarctation repair still have an increased risk of cardiovascular or cerebrovascular events. This has been explained by the persisting hypertension and alterations in the peripheral vessels. However, involvement of the central vessels such as the retinal arteries is virtually unknown. A total of 34 patients after coarctation repair (22 men and 12 women; 23 to 58 years old, age range 0 to 32 years at surgical repair) and 34 nonhypertensive controls underwent structural and functional retinal vessel analysis. Using structural analysis, the vessel diameters were measured. Using functional analysis, the endothelium-dependent vessel dilation in response to flicker light stimulation was assessed. In the patients after coarctation repair, the retinal arteriolar diameter was significantly reduced compared to that of the controls (median 182 μm, first to third quartile 171 to 197; vs 197 μm, first to third quartile 193 to 206; p <0.001). These findings were independent of the peripheral blood pressure and age at intervention. No differences were found for venules. The functional analysis findings were not different between the patients and controls (maximum dilation 3.5\%, first to third quartile 2.1\% to 4.5\% vs 3.6\%, first to third quartile 2.2\% to 4.3\%; p = 0.81), indicating preserved autoregulative mechanisms. In conclusion, the retinal artery diameter is reduced in patients after coarctation repair, independent of their current blood pressure level and age at intervention. As a structural marker of chronic vessel damage associated with past, current, or future hypertension, retinal arteriolar narrowing has been linked to stroke incidence. These results indicate an involvement of cerebral microcirculation in aortic coarctation, despite timely repair, and might contribute to explain the increased rate of cerebrovascular events in such patients.},
  language  = {en}
}