Alpha-synuclein and neurodegenerative diseases
By M. Goedert. Nature Reviews Neuroscience, 2001
1,401 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Neurology
View Paper: https://www.semanticscholar.org/paper/b7ff091064be6b2c655167f23f5013cb39a3c2fa
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cellular and Molecular Neuroscience
- Fred H. Gage
- H. Ko
- Sebastian Jessberger
- Valina L. Dawson
- T. Dawson
- A. Consiglio
- K. Del Tredici
- S. Przedborski
In Neurology
Citations in the corpus
- Neurodegenerative disease and adult neurogenesis (2011, background): “Loss of DAergic neurons in the substantia nigra of the midbrain and loss of other neurotransmitter phenotype neurons in other brain regions are characteristic neuropathological hallmarks (reviewed in Goedert, 2001).”
- Staging of the intracerebral inclusion body pathology associated with idiopathic Parkinson's disease (preclinical and clinical stages) (2002, background): “LNs/LBs consist mainly of aggregations of a misfolded, for the most part normally presynaptic protein, α-synuclein [7, 11, 13, 16, 17, 19, 21].”
- Hallmarks of neurodegenerative diseases. (2023, neutral): “…involved (i.e., nuclear, cytoplasmic, and pre-or post-synaptic), enabling their interference with different NDD hallmarks (outlined below), 7,10,12,14,19,21,22,24,25,27,44,64–67 (Figures 1 and 3), although the exact toxic mechanism and the toxic forms of these aggregates have not yet been…”
- Parkinson's Disease Mechanisms and Models (2003, background): “A growing literature supports this notion and links the pathogenesis ofbeen found in brains from patients with either mutation, although some atypical features have also been noted PD to other neurodegenerative diseases that involve protein aggregation (reviewed by Goedert, 2001).”
- Prion-like spreading of pathological α-synuclein in brain (2013, background): “Filamentous inclusions composed of -synuclein in nerve cells or glial cells are the defining neuropathological feature of a group of neurodegenerative diseases including Parkinson’s disease, dementia with Lewy bodies, and multiple-system atrophy (Goedert, 2001).”
- In vivo demonstration that α-synuclein oligomers are toxic (2011, background): “Prominent neuropathological hallmarks of PD are the loss of dopaminergic neurons in the substantia nigra (SN) region of the midbrain (1) and the presence of α-syn–containing intracellular inclusions: Lewy bodies (LBs) and Lewy neurites (2).”
- Intravesicular Localization and Exocytosis of α-Synuclein and its Aggregates (2005, background): “Fibrillar aggregates of -synuclein ( -syn) constitute a major component of these intracellular inclusions and are also found in many other neurological disorders, including dementia with Lewy bodies and multiple system atrophy (Goedert, 2001).”
- Different Species of α-Synuclein Oligomers Induce Calcium Influx and Seeding (2007, background): “The main component of these intracellular deposits is aggregated -synuclein ( -syn) (Goedert, 2001).”
- Copper in diseases and treatments, and copper‐based anticancer strategies (2009, background): “Since this discovery, the process of AS aggregation has been proposed to underlie dopaminergic degeneration in PD.(119) Altered metal homeostasis has been described as an important cofactor in the progression of PD.”
- Genetic Animal Models of Parkinson’s Disease (2010, positive): “It was the genetic discovery of a-synuclein linkage to PD that led to the discovery that a-synuclein was the major structural moiety of Lewy bodies and neurites (Goedert, 2001).”