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  •   Ιδρυματικό Αποθετήριο Πανεπιστημίου Θεσσαλίας
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  •   Ιδρυματικό Αποθετήριο Πανεπιστημίου Θεσσαλίας
  • Επιστημονικές Δημοσιεύσεις Μελών ΠΘ (ΕΔΠΘ)
  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ.
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Ιδρυματικό Αποθετήριο Πανεπιστημίου Θεσσαλίας
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Mitochondrial dynamics and proteins related to neurodegenerative diseases

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Συγγραφέας
Alexiou A., Nizami B., Khan F.I., Soursou G., Vairaktarakis C., Chatzichronis S., Tsiamis V., Manztavinos V., Yarla N.S., Md Ashraf G.
Ημερομηνία
2018
Γλώσσα
en
DOI
10.2174/1389203718666170810150151
Λέξη-κλειδί
alpha synuclein
amyloid beta protein
parkin
reactive oxygen metabolite
ubiquitin protein ligase
cell death
degenerative disease
human
metabolism
mitochondrial dynamics
mitochondrion
nerve cell
physiology
protein conformation
protein folding
alpha-Synuclein
Amyloid beta-Peptides
Cell Death
Humans
Mitochondria
Mitochondrial Dynamics
Neurodegenerative Diseases
Neurons
Protein Conformation
Protein Folding
Reactive Oxygen Species
Ubiquitin-Protein Ligases
Bentham Science Publishers B.V.
Εμφάνιση Μεταδεδομένων
Επιτομή
Disruptions in the regulation of mitochondrial dynamics and the occurrence of proteins misfolding lead to neuronal death, resulting in Age-related Dementia and Neurodegenerative diseases as well as Frailty. Functional, neurophysiologic and biochemical alterations within the mitochondrial populations can reveal deficits in brain energy metabolism resulting in Mild Cognitive Impairment, abnormal neural development, autonomic dysfunction and other mitochondrial disorders. Additionally, in cases of Alzheimer’s disease or Parkinson’s disease, a significant number of proteins seem to form unordered and problematic structures, leading through unknown mechanisms to pathological conditions. While the proteins structure prediction problem is still an open challenge regarding its complexity, several features associated with the correlations of misfolding proteins and Neurodegeneration are discussed in the present study and a computational analysis for the proteins Amyloid Beta, Tau, α-Synuclein, Parkin, Pink1, MFN1, MFN1, OPA1, and DNM1L is also presented. © 2018 Bentham Science Publishers.
URI
http://hdl.handle.net/11615/70418
Collections
  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ. [19735]

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