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Acute decrease in alkaline phosphatase after brain injury: A potential mechanism for tauopathy.

Peethambaran Arun1, Samuel Oguntayo1, Stephen Van Albert1

  • 1Blast-Induced Neurotrauma Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research, Silver Spring, MD 20910, USA.

Neuroscience Letters
|October 21, 2015
PubMed
Summary
This summary is machine-generated.

Traumatic brain injuries decrease tissue non-specific alkaline phosphatase (TNAP) activity, leading to phosphorylated Tau (pTau) accumulation and tauopathy. This suggests a distinct mechanism from Alzheimer's disease in TBI-induced tauopathy.

Keywords:
Blast exposureChronic traumatic encephalopathyHead impact/accelerationTauopathyTissue non-specific alkaline phosphataseTraumatic brain injury

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Phosphorylated Tau (pTau) protein is crucial for neuronal microtubule stability and protection against tauopathy.
  • Tissue non-specific alkaline phosphatase (TNAP) is the primary enzyme responsible for pTau dephosphorylation in the brain.
  • Hyperphosphorylated Tau in Alzheimer's disease (AD) prevents microtubule assembly, highlighting the importance of dephosphorylation.

Purpose of the Study:

  • To investigate the relationship between traumatic brain injury (TBI) and the activity of TNAP.
  • To determine the impact of TBI on pTau accumulation and subsequent tauopathy.
  • To explore the potential distinction between TBI-induced tauopathy and AD mechanisms.

Main Methods:

  • Utilized blast and weight drop models to induce TBI in rats.
  • Monitored pTau accumulation at 6h and 24h post-injury.
  • Assessed TNAP expression and activity in affected brain regions.
  • Measured plasma total alkaline phosphatase activity.

Main Results:

  • pTau accumulation was observed as early as 6h post-TBI, with regional variations by 24h.
  • TBI led to reduced TNAP expression and activity in brain regions with pTau accumulation.
  • Significantly decreased plasma total alkaline phosphatase activity was noted after TBI.
  • No correlation was found between TNAP/pTau changes and amyloid precursor protein accumulation.

Conclusions:

  • Blast and impact acceleration-induced head injuries acutely decrease brain TNAP levels/activity.
  • This decrease in TNAP activity may contribute to trauma-induced pTau accumulation and tauopathy.
  • The mechanisms of tauopathy in TBI appear distinct from those in AD, as indicated by the lack of correlation with amyloid precursor protein.