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Avila J, Perry G, Strange BA, et al. Alternative neural circuitry that might be impaired in the development of Alzheimer disease. Front Neurosci. 2015;9:145doi: 10.3389/fnins.2015.00145.
Avila, J., Perry, G., Strange, B. A., & Hernandez, F. (2015). Alternative neural circuitry that might be impaired in the development of Alzheimer disease. Frontiers in neuroscience, 9145. https://doi.org/10.3389/fnins.2015.00145
Avila, Jesus, et al. "Alternative neural circuitry that might be impaired in the development of Alzheimer disease." Frontiers in neuroscience vol. 9 (2015): 145. doi: https://doi.org/10.3389/fnins.2015.00145
Avila J, Perry G, Strange BA, Hernandez F. Alternative neural circuitry that might be impaired in the development of Alzheimer disease. Front Neurosci. 2015 Apr 23;9:145. doi: 10.3389/fnins.2015.00145. eCollection 2015. PMID: 25954151; PMCID: PMC4407584.
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Front Neurosci. 2015 Apr 23;9:145. doi: 10.3389/fnins.2015.00145. eCollection 2015.

Alternative neural circuitry that might be impaired in the development of Alzheimer disease.

Frontiers in neuroscience

Jesus Avila, George Perry, Bryan A Strange, Felix Hernandez

Affiliations

  1. Neurobiology, Centro de Biologia Molecular Severo Ochoa (CSIC-UAM) Madrid, Spain ; Centro de Investigacion Biomedica en Red de Enfermedades Neurodegenerativas Madrid, Spain.
  2. College of Sciences, The University of Texas at San Antonio San Antonio, TX, USA.
  3. Department of Neuroimaging, Reina Sofia Foundation, Center for Alzheimer Research, FCIEN Madrid, Spain ; Laboratory for Clinical Neuroscience, CTB, Universidad Politecnica de Madrid Madrid, Spain.

PMID: 25954151 PMCID: PMC4407584 DOI: 10.3389/fnins.2015.00145

Abstract

It is well established that some individuals with normal cognitive capacity have abundant senile plaques in their brains. It has been proposed that those individuals are resilient or have compensation factors to prevent cognitive decline. In this comment, we explore an alternative mechanism through which cognitive capacity is maintained. This mechanism could involve the impairment of alternative neural circuitry. Also, the proportion of molecules such as Aβ or tau protein present in different areas of the brain could be important.

Keywords: Alzheimer disease (AD); abeta; cognitive decline; tau proteins; tauopathies

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