@article{AmmarThahoulyHanaueretal.2015,
  author    = {Ammar, Mohamed Raafet and Thahouly, Tamou and Hanauer, Andr{\´e} and Stegner, David and Nieswandt, Bernhard and Vitale, Nicolas},
  title     = {PLD1 participates in BDNF-induced signalling in cortical neurons},
  series = {Scientific Reports},
  volume    = {5},
  journal   = {Scientific Reports},
  number    = {14778},
  doi       = {10.1038/srep14778},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-139962},
  year      = {2015},
  abstract  = {The brain-derived neurotrophic factor BDNF plays a critical role in neuronal development and the induction of L-LTP at glutamatergic synapses in several brain regions. However, the cellular and molecular mechanisms underlying these BDNF effects have not been firmly established. Using in vitro cultures of cortical neurons from knockout mice for Pld1 and Rsk2, BDNF was observed to induce a rapid RSK2-dependent activation of PLD and to stimulate BDNF ERK1/2-CREB and mTor-S6K signalling pathways, but these effects were greatly reduced in Pld1\(^{-/-}\) neurons. Furthermore, phospho-CREB did not accumulate in the nucleus, whereas overexpression of PLD1 amplified the BDNF-dependent nuclear recruitment of phospho-ERK1/2 and phospho-CREB. This BDNF retrograde signalling was prevented in cells silenced for the scaffolding protein PEA15, a protein which complexes with PLD1, ERK1/2, and RSK2 after BDNF treatment. Finally PLD1, ERK1/2, and RSK2 partially colocalized on endosomal structures, suggesting that these proteins are part of the molecular module responsible for BDNF signalling in cortical neurons.},
  language  = {en}
}
@article{KimFranckKangetal.2015,
  author    = {Kim, Jae Ho and Franck, Julien and Kang, Taewook and Heinsen, Helmut and Ravid, Rivka and Ferrer, Isidro and Cheon, Mi Hee and Lee, Joo-Yong and Yoo, Jong Shin and Steinbusch, Harry W. and Salzet, Michel and Fournier, Isabelle and Park, Young Mok},
  title     = {Proteome-wide characterization of signalling interactions in the hippocampal CA4/DG subfield of patients with Alzheimer's disease},
  series = {Scientific Reports},
  volume    = {5},
  journal   = {Scientific Reports},
  number    = {11138},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-151727},
  year      = {2015},
  abstract  = {Alzheimer's disease (AD) is the most common form of dementia; however, mechanisms and biomarkers remain unclear. Here, we examined hippocampal CA4 and dentate gyrus subfields, which are less studied in the context of AD pathology, in post-mortem AD and control tissue to identify possible biomarkers. We performed mass spectrometry-based proteomic analysis combined with label-free quantification for identification of differentially expressed proteins. We identified 4,328 proteins, of which 113 showed more than 2-fold higher or lower expression in AD hippocampi than in control tissues. Five proteins were identified as putative AD biomarkers (MDH2, PCLO, TRRAP, YWHAZ, and MUC19 isoform 5) and were cross-validated by immunoblotting, selected reaction monitoring, and MALDI imaging. We also used a bioinformatics approach to examine upstream signalling interactions of the 113 regulated proteins. Five upstream signalling (IGF1, BDNF, ZAP70, MYC, and cyclosporin A) factors showed novel interactions in AD hippocampi. Taken together, these results demonstrate a novel platform that may provide new strategies for the early detection of AD and thus its diagnosis.},
  language  = {en}
}
@article{FoersterShityakovScheperetal.2022,
  author    = {F{\"o}rster, Carola Y. and Shityakov, Sergey and Scheper, Verena and Lenarz, Thomas},
  title     = {Linking cerebrovascular dysfunction to age-related hearing loss and Alzheimer's disease — are systemic approaches for diagnosis and therapy required?},
  series = {Biomolecules},
  volume    = {12},
  journal   = {Biomolecules},
  number    = {11},
  issn      = {2218-273X},
  doi       = {10.3390/biom12111717},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-297552},
  year      = {2022},
  abstract  = {Alzheimer's disease (AD), the most common cause of dementia in the elderly, is a neurodegenerative disorder associated with neurovascular dysfunction, cognitive decline, and the accumulation of amyloid β peptide (Aβ) in the brain and tau-related lesions in neurons termed neurofibrillary tangles (NFTs). Aβ deposits and NFT formation are the central pathological hallmarks in AD brains, and the majority of AD cases have been shown to exhibit a complex combination of systemic comorbidities. While AD is the foremost common cause of dementia in the elderly, age-related hearing loss (ARHL) is the most predominant sensory deficit in the elderly. During aging, chronic inflammation and resulting endothelial dysfunction have been described and might be key contributors to AD; we discuss an intriguing possible link between inner ear strial microvascular pathology and blood-brain barrier pathology and present ARHL as a potentially modifiable and treatable risk factor for AD development. We present compelling evidence that ARHL might well be seen as an important risk factor in AD development: progressive hearing impairment, leading to social isolation, and its comorbidities, such as frailty, falls, and late-onset depression, link ARHL with cognitive decline and increased risk of dementia, rendering it tempting to speculate that ARHL might be a potential common molecular and pathological trigger for AD. Additionally, one could speculate that amyloid-beta might damage the blood-labyrinth barrier as it does to the blood-brain barrier, leading to ARHL pathology. Finally, there are options for the treatment of ARHL by targeted neurotrophic factor supplementation to the cochlea to improve cognitive outcomes; they can also prevent AD development and AD-related comorbidity in the future.},
  language  = {en}
}