Abstract
Along the last years it has been demonstrated that non-neural cells play a major role in the pathogenesis of the primary degenerative disorders (PDDs) of the human central nervous system. Among them, astrocytes coordinate and participate in many different and complex metabolic processes, in close interaction with neurons. Moreover, increasing experimental evidence hints an early astrocytic dysfunction in these diseases. In this mini review we summarize the astrocytic behavior in PDDs, with special consideration to the experimental observations where astrocytic pathology precedes the development of neuronal dysfunction. We also suggest a different approach that could be consider in human investigations in Alzheimer’s and Parkinson’s disease. We believe that the study of PDDs with human brain samples may hold the key of a paradigmatic physiopathological process in which astrocytes might be the main players.
Highlights
Reviewed by: Anna Maria Colangelo, University of Milano-Bicocca, Italy Christiane Charriaut-Marlangue, Institut National de la Santé et de la Recherche Médicale, France
Increasing experimental evidence hints an early astrocytic dysfunction in these diseases. In this mini review we summarize the astrocytic behavior in primary degenerative disorders (PDDs), with special consideration to the experimental observations where astrocytic pathology precedes the development of neuronal dysfunction
In the present mini review, this concept has been exemplified in CNS at its whole length: starting in the spine or the brain stem in amyotrophic lateral sclerosis (ALS) patients, ascending to the midbrain in Parkinson disease (PD), the cerebellum in Spinocerebellar Ataxia (SCA)-7, the striatum in Huntington’s Disease (HD), the hippocampus in Alzheimer disease (AD), the prefrontal cortex in frontotemporal dementia (FTD) and, compromising in a more subtle fashion the whole cortical gray matter in SCZ
Summary
A particular difficulty in the study of these diseases is that they mostly represent a deterioration of a highly evolved cognitive and/or motor functioning system. Punctually in psychiatric illnesses, it seems that animal models are far from resembling all the peculiarities of the human diseases, even if the anatomopathological findings can be mimicked. Human testing is ethically inappropriate for obvious reasons and the most representative research tool available is the study of post mortem human brains (Harrison, 1999; Broadstock et al, 2014). Since clinical diagnosis relies in a constellation of signs and symptoms that are secondary to a physiopathogenic process that is far from recently starting, the study of the disease early-stages is extremely difficult. All the above determines hazards to the methodological study approach of many hypotheses, those involving disease onset and progression
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