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Glymphatic System Impairment in Alzheimer's Disease and Idiopathic Normal Pressure Hydrocephalus

Reeves, Benjamin C. ; Karimy, Jason K. ; Kundishora, Adam J. ; Mestre, Humberto ; Cerci, H. Mert ; Matouk, Charles ; Alper, Seth L. ; Lundgaard, Iben LU ; Nedergaard, Maiken and Kahle, Kristopher T. (2020) In Trends in Molecular Medicine 26(3). p.285-295
Abstract

Approximately 10% of dementia patients have idiopathic normal pressure hydrocephalus (iNPH), an expansion of the cerebrospinal fluid (CSF)-filled brain ventricles. iNPH and Alzheimer's disease (AD) both exhibit sleep disturbances, build-up of brain metabolic wastes and amyloid-β (Aβ) plaques, perivascular reactive astrogliosis, and mislocalization of astrocyte aquaporin-4 (AQP4). The glia–lymphatic (glymphatic) system facilitates brain fluid clearance and waste removal during sleep via glia-supported perivascular channels. Human studies have implicated impaired glymphatic function in both AD and iNPH. Continued investigation into the role of glymphatic system biology in AD and iNPH models could lead to new strategies to improve brain... (More)

Approximately 10% of dementia patients have idiopathic normal pressure hydrocephalus (iNPH), an expansion of the cerebrospinal fluid (CSF)-filled brain ventricles. iNPH and Alzheimer's disease (AD) both exhibit sleep disturbances, build-up of brain metabolic wastes and amyloid-β (Aβ) plaques, perivascular reactive astrogliosis, and mislocalization of astrocyte aquaporin-4 (AQP4). The glia–lymphatic (glymphatic) system facilitates brain fluid clearance and waste removal during sleep via glia-supported perivascular channels. Human studies have implicated impaired glymphatic function in both AD and iNPH. Continued investigation into the role of glymphatic system biology in AD and iNPH models could lead to new strategies to improve brain health by restoring homeostatic brain metabolism and CSF dynamics.

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organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
aging, Alzheimer's disease, dementia, glial-lymphatic, glymphatic, hydrocephalus, idiopathic normal pressure hydrocephalus
in
Trends in Molecular Medicine
volume
26
issue
3
pages
11 pages
publisher
Elsevier
external identifiers
  • scopus:85077932270
  • pmid:31959516
ISSN
1471-4914
DOI
10.1016/j.molmed.2019.11.008
language
English
LU publication?
yes
id
299f3cd7-1e84-460f-8928-66d405753c4f
date added to LUP
2020-01-30 14:29:38
date last changed
2024-06-13 10:35:49
@article{299f3cd7-1e84-460f-8928-66d405753c4f,
  abstract     = {{<p>Approximately 10% of dementia patients have idiopathic normal pressure hydrocephalus (iNPH), an expansion of the cerebrospinal fluid (CSF)-filled brain ventricles. iNPH and Alzheimer's disease (AD) both exhibit sleep disturbances, build-up of brain metabolic wastes and amyloid-β (Aβ) plaques, perivascular reactive astrogliosis, and mislocalization of astrocyte aquaporin-4 (AQP4). The glia–lymphatic (glymphatic) system facilitates brain fluid clearance and waste removal during sleep via glia-supported perivascular channels. Human studies have implicated impaired glymphatic function in both AD and iNPH. Continued investigation into the role of glymphatic system biology in AD and iNPH models could lead to new strategies to improve brain health by restoring homeostatic brain metabolism and CSF dynamics.</p>}},
  author       = {{Reeves, Benjamin C. and Karimy, Jason K. and Kundishora, Adam J. and Mestre, Humberto and Cerci, H. Mert and Matouk, Charles and Alper, Seth L. and Lundgaard, Iben and Nedergaard, Maiken and Kahle, Kristopher T.}},
  issn         = {{1471-4914}},
  keywords     = {{aging; Alzheimer's disease; dementia; glial-lymphatic; glymphatic; hydrocephalus; idiopathic normal pressure hydrocephalus}},
  language     = {{eng}},
  month        = {{03}},
  number       = {{3}},
  pages        = {{285--295}},
  publisher    = {{Elsevier}},
  series       = {{Trends in Molecular Medicine}},
  title        = {{Glymphatic System Impairment in Alzheimer's Disease and Idiopathic Normal Pressure Hydrocephalus}},
  url          = {{http://dx.doi.org/10.1016/j.molmed.2019.11.008}},
  doi          = {{10.1016/j.molmed.2019.11.008}},
  volume       = {{26}},
  year         = {{2020}},
}