@article{JeglinskiMende2019,
  author    = {Jeglinski-Mende, Melinda A.},
  title     = {Alcohol in the Aging Brain},
  series = {Frontiers in Neuroscience},
  volume    = {13},
  journal   = {Frontiers in Neuroscience},
  publisher = {Frontiers Research Foundation},
  address   = {Lausanne},
  issn      = {1662-453X},
  doi       = {10.3389/fnins.2019.00713},
  pages     = {7},
  year      = {2019},
  abstract  = {As our society grows older new challenges for medicine and healthcare emerge. Agerelated changes of the body have been observed in essential body functions, particularly in the loco-motor system, in the cardiovascular system and in cognitive functions concerning both brain plasticity and changes in behavior. Nutrition and lifestyle, such as nicotine intake and chronic alcohol consumption, also contribute to biological changes in the brain. This review addresses the effect of alcohol consumption on cognitive decline, changes in brain plasticity in the aging brain and on cardiovascular health in aging. Thus, studies on the interplay of chronic alcohol intake and either cognitive decline or cognitive preservation are outlined. Because of the inconsistency in the literature of whether alcohol consumption preserves cognitive functions in the aging brain or whether it accelerates cognitive decline, it is crucial to consider individual contributing factors such as culture, health and lifestyle in future studies.},
  language  = {en}
}
@misc{JeglinskiMende2019,
  author    = {Jeglinski-Mende, Melinda A.},
  title     = {Alcohol in the aging brain},
  series = {Frontiers in neuroscience},
  volume    = {13},
  journal   = {Frontiers in neuroscience},
  publisher = {Frontiers Research Foundation},
  address   = {Lausanne},
  issn      = {1662-453X},
  doi       = {10.3389/fnins.2019.00713},
  pages     = {7},
  year      = {2019},
  abstract  = {As our society grows older new challenges for medicine and healthcare emerge. Age-related changes of the body have been observed in essential body functions, particularly in the loco-motor system, in the cardiovascular system and in cognitive functions concerning both brain plasticity and changes in behavior. Nutrition and lifestyle, such as nicotine intake and chronic alcohol consumption, also contribute to biological changes in the brain. This review addresses the effect of alcohol consumption on cognitive decline, changes in brain plasticity in the aging brain and on cardiovascular health in aging. Thus, studies on the interplay of chronic alcohol intake and either cognitive decline or cognitive preservation are outlined. Because of the inconsistency in the literature of whether alcohol consumption preserves cognitive functions in the aging brain or whether it accelerates cognitive decline, it is crucial to consider individual contributing factors such as culture, health and lifestyle in future studies.},
  language  = {en}
}
@article{KlausMuellervanWickerenetal.2022,
  author    = {Klaus, Benita and M{\"u}ller, Patrick and van Wickeren, Nora and Dordevic, Milos and Schmicker, Marlen and Zdunczyk, Yael and Brigadski, Tanja and Lessmann, Volkmar and Vielhaber, Stefan and Schreiber, Stefanie and M{\"u}ller, Notger G.},
  title     = {Structural and functional brain alterations in patients with myasthenia gravis},
  series = {Brain communications},
  volume    = {4},
  journal   = {Brain communications},
  number    = {1},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  issn      = {2632-1297},
  doi       = {10.1093/braincomms/fcac018},
  pages     = {12},
  year      = {2022},
  abstract  = {Myasthenia gravis is an autoimmune disease affecting neuromuscular transmission and causing skeletal muscle weakness. Additionally, systemic inflammation, cognitive deficits and autonomic dysfunction have been described. However, little is known about myasthenia gravis-related reorganization of the brain. In this study, we thus investigated the structural and functional brain changes in myasthenia gravis patients. Eleven myasthenia gravis patients (age: 70.64 +/- 9.27; 11 males) were compared to age-, sex- and education-matched healthy controls (age: 70.18 +/- 8.98; 11 males). Most of the patients (n = 10, 0.91\%) received cholinesterase inhibitors. Structural brain changes were determined by applying voxel-based morphometry using high-resolution T-1-weighted sequences. Functional brain changes were assessed with a neuropsychological test battery (including attention, memory and executive functions), a spatial orientation task and brain-derived neurotrophic factor blood levels. Myasthenia gravis patients showed significant grey matter volume reductions in the cingulate gyrus, in the inferior parietal lobe and in the fusiform gyrus. Furthermore, myasthenia gravis patients showed significantly lower performance in executive functions, working memory (Spatial Span, P = 0.034, d = 1.466), verbal episodic memory (P = 0.003, d = 1.468) and somatosensory-related spatial orientation (Triangle Completion Test, P = 0.003, d = 1.200). Additionally, serum brain-derived neurotrophic factor levels were significantly higher in myasthenia gravis patients (P = 0.001, d = 2.040). Our results indicate that myasthenia gravis is associated with structural and functional brain alterations. Especially the grey matter volume changes in the cingulate gyrus and the inferior parietal lobe could be associated with cognitive deficits in memory and executive functions. Furthermore, deficits in somatosensory-related spatial orientation could be associated with the lower volumes in the inferior parietal lobe. Future research is needed to replicate these findings independently in a larger sample and to investigate the underlying mechanisms in more detail. Klaus et al. compared myasthenia gravis patients to matched healthy control subjects and identified functional alterations in memory functions as well as structural alterations in the cingulate gyrus, in the inferior parietal lobe and in the fusiform gyrus.},
  language  = {en}
}
@article{WiebkingLinWippert2022,
  author    = {Wiebking, Christine and Lin, Chiao-I and Wippert, Pia-Maria},
  title     = {Training intervention effects on cognitive performance and neuronal plasticity — A pilot study},
  series = {Frontiers in Neurology, section Neurorehabilitation},
  volume    = {13},
  journal   = {Frontiers in Neurology, section Neurorehabilitation},
  publisher = {Frontiers},
  address   = {Lausanne, Schweiz},
  issn      = {1664-2295},
  doi       = {10.3389/fneur.2022.773813},
  pages     = {11},
  year      = {2022},
  abstract  = {Studies suggest that people suffering from chronic pain may have altered brain plasticity, along with altered functional connectivity between pain-processing brain regions. These may be related to decreased mood and cognitive performance. There is some debate as to whether physical activity combined with behavioral therapy (e.g. cognitive distraction, body scan) may counteract these changes. However, underlying neuronal mechanisms are unclear. The aim of the current pilot study with a 3-armed randomized controlled trial design was to examine the effects of sensorimotor training for nonspecific chronic low back pain on (1) cognitive performance; (2) fMRI activity co-fluctuations (functional connectivity) between pain-related brain regions; and (3) the relationship between functional connectivity and subjective variables (pain and depression). Six hundred and sixty two volunteers with non-specific chronic low back pain were randomly allocated to a unimodal (sensorimotor training), multidisciplinary (sensorimotor training and behavioral therapy) intervention, or to a control group within a multicenter study. A subsample of patients (n = 21) from one study center participated in the pilot study presented here. Measurements were at baseline, during (3 weeks, M2) and after intervention (12 weeks, M4 and 24 weeks, M5). Cognitive performance was measured by the Trail Making Test and functional connectivity by MRI. Pain perception and depression were assessed by the Von Korff questionnaire and the Hospital and Anxiety. Group differences were calculated by univariate and repeated ANOVA measures and Bayesian statistics; correlations by Pearson's r. Change and correlation of functional connection were analyzed within a pooled intervention group (uni-, multidisciplinary group). Results revealed that participants with increased pain intensity at baseline showed higher functional connectivity between pain-related brain areas used as ROIs in this study. Though small sample sizes limit generalization, cognitive performance increased in the multimodal group. Increased functional connectivity was observed in participants with increased pain ratings. Pain ratings and connectivity in pain-related brain regions decreased after the intervention. The results provide preliminary indication that intervention effects can potentially be achieved on the cognitive and neuronal level. The intervention may be suitable for therapy and prevention of non-specific chronic low back pain.},
  language  = {en}
}
@article{WippertWiebking2018,
  author    = {Wippert, Pia-Maria and Wiebking, Christine},
  title     = {Stress and Alterations in the Pain Matrix},
  series = {International Journal of Environmental Research and Public Health},
  volume    = {15},
  journal   = {International Journal of Environmental Research and Public Health},
  number    = {4},
  publisher = {MDPI AG},
  address   = {Basel},
  issn      = {1660-4601},
  doi       = {10.3390/ijerph15040785},
  pages     = {1 -- 11},
  year      = {2018},
  abstract  = {The genesis of chronic pain is explained by a biopsychosocial model. It hypothesizes an interdependency between environmental and genetic factors provoking aberrant long-term changes in biological and psychological regulatory systems. Physiological effects of psychological and physical stressors may play a crucial role in these maladaptive processes. Specifically, long-term demands on the stress response system may moderate central pain processing and influence descending serotonergic and noradrenergic signals from the brainstem, regulating nociceptive processing at the spinal level. However, the underlying mechanisms of this pathophysiological interplay still remain unclear. This paper aims to shed light on possible pathways between physical (exercise) and psychological stress and the potential neurobiological consequences in the genesis and treatment of chronic pain, highlighting evolving concepts and promising research directions in the treatment of chronic pain. Two treatment forms (exercise and mindfulness-based stress reduction as exemplary therapies), their interaction, and the dose-response will be discussed in more detail, which might pave the way to a better understanding of alterations in the pain matrix and help to develop future prevention and therapeutic concepts},
  language  = {en}
}