Neurobiology of Disease

Journal: Neurobiology of Disease

Abbreviation

Neurobiol. Dis.

Publisher

Elsevier

ISSN

0969-9961
1095-953X

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Publications 1 - 10 of 11

Distinct disease mechanisms in peripheral neuropathies due to altered peripheral myelin protein 22 gene dosage or a Pmp22 point mutation
Giambonini-Brugnoli, Guya; Buchstaller, Johanna; Sommer, Lukas; et al. (2005)
Neurobiology of Disease
Epigenetic inheritance in mammals
Franklin, Tamara B.; Mansuy, Isabelle (2010)
Neurobiology of Disease
Long-distance axonal regeneration induced by CNTF gene transfer is impaired by axonal misguidance in the injured adult optic nerve
Pernet, Vincent; Joly, Sandrine; Dalkara, Deniz; et al. (2013)
Neurobiology of Disease
The modulatory effect of self-paced and cued motor execution on subthalamic beta-bursts in Parkinson's disease: Evidence from deep brain recordings in humans
Bichsel, Oliver; Stieglitz, Lennart; Oertel, Markus; et al. (2022)
Neurobiology of Disease
Deep brain stimulation (DBS) electrodes provide an unparalleled window to record and investigate neuronal activity right at the core of pathological brain circuits. In Parkinson's disease (PD), basal ganglia beta-oscillatory activity (13–35 Hz) seems to play an outstanding role. Conventional DBS, which globally suppresses beta-activity, does not meet the requirements of a targeted treatment approach given the intricate interplay of physiological and pathological effects of beta-frequencies. Here, we wanted to characterise the local field potential (LFP) in the subthalamic nucleus (STN) in terms of beta-burst prevalence, amplitude and length between movement and rest as well as during self-paced as compared to goal-directed motor control. Our electrophysiological recordings from externalised DBS-electrodes in nine patients with PD showed a marked decrease in beta-burst durations and prevalence during movement as compared to rest as well as shorter and less frequent beta-bursts during cued as compared to self-paced movements. These results underline the importance of beta-burst modulation in movement generation and are in line with the clinical observation that cued motor control is better preserved than self-paced movements. Furthermore, our findings motivate the use of adaptive DBS based on beta-bursts, which selectively trim longer beta-bursts, as it is more suitable and efficient over a range of motor behaviours than conventional DBS.
Increased plasma bradykinin level is associated with cognitive impairment in Alzheimer's patients
Singh, Pradeep K.; Chen, Zu-Lin; Ghosh, Dhiman; et al. (2020)
Neurobiology of Disease
Alzheimer's disease (AD) is characterized by the presence of proteinaceous brain deposits, brain atrophy, vascular dysfunction, and chronic inflammation. Along with cerebral inflammation, peripheral inflammation is also evident in many AD patients. Bradykinin, a proinflammatory plasma peptide, is also linked to AD pathology. For example, bradykinin infusion into the hippocampus causes learning and memory deficits in rats, and blockade of the bradykinin receptor lessens cognitive impairment in AD mouse models. Even though it has been hypothesized that plasma bradykinin could contribute to inflammation in AD, the level of plasma bradykinin and its association with beta-amyloid (Aβ) pathology in AD patients had not been explored. Here, we assessed plasma bradykinin levels in AD patients and age-matched non-demented (ND) control individuals. We found significantly elevated plasma bradykinin levels in AD patients compared to ND subjects. Additionally, changes in plasma bradykinin levels were more profound in many AD patients with severe cognitive impairment, suggesting that peripheral bradykinin could play a role in dementia most likely via inflammation. Bradykinin levels in the cerebrospinal fluid (CSF) were reduced in AD patients and exhibited an inverse correlation with the CSF Aβ40/Aβ42 ratio. We also report that bradykinin interacts with the fibrillar form of Aβ and co-localizes with Aβ plaques in the post-mortem human AD brain. These findings connect the peripheral inflammatory pathway to cerebral abnormalities and identify a novel mechanism of inflammatory pathology in AD.
ApoE4 impairs hippocampal plasticity isoform-specifically and blocks the environmental stimulation of synaptogenesis and memory
Levi, Ofir; Jongen-Relo, Ana L.; Feldon, Joram; et al. (2003)
Neurobiology of Disease
Vascular response to acetazolamide decreases as a function of age in the arcAβ mouse model of cerebral amyloidosis
Princz-Kranz, Felicitas L.; Mueggler, Thomas; Knobloch, Marlen; et al. (2010)
Neurobiology of Disease
Nogo and Nogo receptor
Willi, R.; Schwab, Martin E. (2013)
Neurobiology of Disease
GDAP1 mutations differ in their effects on mitochondrial dynamics and apoptosis depending on the mode of inheritance
Niemann, Axel; Wagner, Konstanze Marion; Rüegg, Marcel; et al. (2009)
Neurobiology of Disease
Neuronal neprilysin overexpression is associated with attenuation of Aβ-related spatial memory deficit
Poirier, Raphael; Wolfer, David Paul; Welzl, Hans; et al. (2006)
Neurobiology of Disease

Publications 1 - 10 of 11

Journal: Neurobiology of Disease

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