Next Article in Journal
The Potential of Targeting Brain Pathology with Ascl1/Mash1
Next Article in Special Issue
Approaches for Studying Autophagy in Caenorhabditis elegans
Previous Article in Journal / Special Issue
Induced Pluripotent Stem Cell Neuronal Models for the Study of Autophagy Pathways in Human Neurodegenerative Disease
Article Menu
Issue 3 (September) cover image

Export Article

Open AccessReview
Cells 2017, 6(3), 25;

Assessment of Autophagy in Neurons and Brain Tissue

Centro de Biología Molecular “Severo Ochoa” (CSIC-UAM), C/Nicolas Cabrera 1, Universidad Autonoma Madrid, Madrid 28049, Spain
Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Valderrebollo 5, Madrid 28049, Spain
Author to whom correspondence should be addressed.
Received: 4 July 2017 / Revised: 1 August 2017 / Accepted: 21 August 2017 / Published: 23 August 2017
(This article belongs to the Special Issue Assays to Monitor Autophagy in Model Systems)
Full-Text   |   PDF [499 KB, uploaded 23 August 2017]   |  


Autophagy is a complex process that controls the transport of cytoplasmic components into lysosomes for degradation. This highly conserved proteolytic system involves dynamic and complex processes, using similar molecular elements and machinery from yeast to humans. Moreover, autophagic dysfunction may contribute to a broad spectrum of mammalian diseases. Indeed, in adult tissues, where the capacity for regeneration or cell division is low or absent (e.g., in the mammalian brain), the accumulation of proteins/peptides that would otherwise be recycled or destroyed may have pathological implications. Indeed, such changes are hallmarks of pathologies, like Alzheimer’s, Prion or Parkinson’s disease, known as proteinopathies. However, it is still unclear whether such dysfunction is a cause or an effect in these conditions. One advantage when analysing autophagy in the mammalian brain is that almost all the markers described in different cell lineages and systems appear to be present in the brain, and even in neurons. By contrast, the mixture of cell types present in the brain and the differentiation stage of such neurons, when compared with neurons in culture, make translating basic research to the clinic less straightforward. Thus, the purpose of this review is to describe and discuss the methods available to monitor autophagy in neurons and in the mammalian brain, a process that is not yet fully understood, focusing primarily on mammalian macroautophagy. We will describe some general features of neuronal autophagy that point to our focus on neuropathologies in which macroautophagy may be altered. Indeed, we centre this review around the hypothesis that enhanced autophagy may be able to provide therapeutic benefits in some brain pathologies, like Alzheimer’s disease, considering this pathology as one of the most prevalent proteinopathies. View Full-Text
Keywords: macroautophagy; signalling; mTORC1; PI3K; Alzheimer’s disease; proteinopathies macroautophagy; signalling; mTORC1; PI3K; Alzheimer’s disease; proteinopathies

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Benito-Cuesta, I.; Diez, H.; Ordoñez, L.; Wandosell, F. Assessment of Autophagy in Neurons and Brain Tissue. Cells 2017, 6, 25.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Cells EISSN 2073-4409 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top