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Convergence of Synapses, Endosomes, and Prions in the Biology of Neurodegenerative Diseases.

Gouras, Gunnar LU orcid (2013) In International Journal of Cell Biology 2013.
Abstract
Age-related misfolding and aggregation of disease-linked proteins in selective brain regions is a characteristic of neurodegenerative diseases. Although neuropathological aggregates that characterize these various diseases are found at sites other than synapses, increasing evidence supports the idea that synapses are where the pathogenesis begins. Understanding these diseases is hampered by our lack of knowledge of what the normal functions of these proteins are and how they are affected by aging. Evidence has supported the idea that neurodegenerative disease-linked proteins have a common propensity for prion protein-like cell-to-cell propagation. However, it is not thought that the prion-like quality of these proteins/peptides that allows... (More)
Age-related misfolding and aggregation of disease-linked proteins in selective brain regions is a characteristic of neurodegenerative diseases. Although neuropathological aggregates that characterize these various diseases are found at sites other than synapses, increasing evidence supports the idea that synapses are where the pathogenesis begins. Understanding these diseases is hampered by our lack of knowledge of what the normal functions of these proteins are and how they are affected by aging. Evidence has supported the idea that neurodegenerative disease-linked proteins have a common propensity for prion protein-like cell-to-cell propagation. However, it is not thought that the prion-like quality of these proteins/peptides that allows their cell-to-cell transmission implies a role for human-to-human spread in common age-related neurodegenerative diseases. It will be important to better understand the molecular and cellular mechanisms governing the role of these aggregating proteins in neural function, especially at synapses, how their propagation occurs and how pathogenesis is promoted by aging. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
International Journal of Cell Biology
volume
2013
article number
141083
publisher
Hindawi Limited
external identifiers
  • pmid:24307901
  • scopus:84888863049
  • pmid:24307901
ISSN
1687-8876
DOI
10.1155/2013/141083
language
English
LU publication?
yes
id
9d760420-daaf-44fe-95fa-39d127a4ba48 (old id 4225194)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24307901?dopt=Abstract
date added to LUP
2016-04-01 10:09:59
date last changed
2022-01-25 20:25:34
@article{9d760420-daaf-44fe-95fa-39d127a4ba48,
  abstract     = {{Age-related misfolding and aggregation of disease-linked proteins in selective brain regions is a characteristic of neurodegenerative diseases. Although neuropathological aggregates that characterize these various diseases are found at sites other than synapses, increasing evidence supports the idea that synapses are where the pathogenesis begins. Understanding these diseases is hampered by our lack of knowledge of what the normal functions of these proteins are and how they are affected by aging. Evidence has supported the idea that neurodegenerative disease-linked proteins have a common propensity for prion protein-like cell-to-cell propagation. However, it is not thought that the prion-like quality of these proteins/peptides that allows their cell-to-cell transmission implies a role for human-to-human spread in common age-related neurodegenerative diseases. It will be important to better understand the molecular and cellular mechanisms governing the role of these aggregating proteins in neural function, especially at synapses, how their propagation occurs and how pathogenesis is promoted by aging.}},
  author       = {{Gouras, Gunnar}},
  issn         = {{1687-8876}},
  language     = {{eng}},
  publisher    = {{Hindawi Limited}},
  series       = {{International Journal of Cell Biology}},
  title        = {{Convergence of Synapses, Endosomes, and Prions in the Biology of Neurodegenerative Diseases.}},
  url          = {{https://lup.lub.lu.se/search/files/1618344/4438264}},
  doi          = {{10.1155/2013/141083}},
  volume       = {{2013}},
  year         = {{2013}},
}