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10.1523/JNEUROSCI.3020-14.2014

http://scihub22266oqcxt.onion/10.1523/JNEUROSCI.3020-14.2014
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C4252540!4252540!25471560
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suck abstract from ncbi


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pmid25471560      J+Neurosci 2014 ; 34 (49): 16180-93
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  • Impairment of Glymphatic Pathway Function Promotes Tau Pathology after Traumatic Brain Injury #MMPMID25471560
  • Iliff JJ; Chen MJ; Plog BA; Zeppenfeld DM; Soltero M; Yang L; Singh I; Deane R; Nedergaard M
  • J Neurosci 2014[Dec]; 34 (49): 16180-93 PMID25471560show ga
  • Traumatic brain injury (TBI) is an established risk factor for the early development of dementia, including Alzheimer's disease, and the post-traumatic brain frequently exhibits neurofibrillary tangles comprised of aggregates of the protein tau. We have recently defined a brain-wide network of paravascular channels, termed the ?glymphatic? pathway, along which CSF moves into and through the brain parenchyma, facilitating the clearance of interstitial solutes, including amyloid-?, from the brain. Here we demonstrate in mice that extracellular tau is cleared from the brain along these paravascular pathways. After TBI, glymphatic pathway function was reduced by ?60%, with this impairment persisting for at least 1 month post injury. Genetic knock-out of the gene encoding the astroglial water channel aquaporin-4, which is importantly involved in paravascular interstitial solute clearance, exacerbated glymphatic pathway dysfunction after TBI and promoted the development of neurofibrillary pathology and neurodegeneration in the post-traumatic brain. These findings suggest that chronic impairment of glymphatic pathway function after TBI may be a key factor that renders the post-traumatic brain vulnerable to tau aggregation and the onset of neurodegeneration.
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