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Reactive astrocytosis refers to the response of astrocytes to different insults to the nervous system, whereas astrocytopathy indicates hypertrophy, atrophy\/degeneration and loss of function and pathological remodeling occurring as a primary cause of a disease or as a factor contributing to the development and progression of a particular disease. Reactive astrocytosis secondary to neuron loss and astrocytopathy due to intrinsic alterations of astrocytes occur in neurodegenerative diseases, overlap each other, and, together with astrocyte senescence, contribute to disease\u2010specific astrogliopathy in aging and neurodegenerative diseases with abnormal protein aggregates in old age. In addition to the well\u2010known increase in glial fibrillary acidic protein and other proteins in reactive astrocytes, astrocytopathy is evidenced by deposition of abnormal proteins such as \u03b2\u2010amyloid, hyper\u2010phosphorylated tau, abnormal \u03b1\u2010synuclein, mutated huntingtin, phosphorylated TDP\u201043 and mutated SOD1, and PrP\n                    <jats:sup>res<\/jats:sup>\n                    , in Alzheimer's disease, tauopathies, Lewy body diseases, Huntington's disease, amyotrophic lateral sclerosis and Creutzfeldt\u2010Jakob disease, respectively. Astrocytopathy in these diseases can also be manifested by impaired glutamate transport; abnormal metabolism and release of neurotransmitters; altered potassium, calcium and water channels resulting in abnormal ion and water homeostasis; abnormal glucose metabolism; abnormal lipid and, particularly, cholesterol metabolism; increased oxidative damage and altered oxidative stress responses; increased production of cytokines and mediators of the inflammatory response; altered expression of connexins with deterioration of cell\u2010to\u2010cell networks and transfer of gliotransmitters; and worsening function of the blood brain barrier, among others. Increased knowledge of these aspects will permit a better understanding of brain aging and neurodegenerative diseases in old age as complex disorders in which neurons are not the only players.\n                  <\/jats:p>","DOI":"10.1111\/bpa.12538","type":"journal-article","created":{"date-parts":[[2017,8,14]],"date-time":"2017-08-14T00:25:12Z","timestamp":1502670312000},"page":"645-674","source":"Crossref","is-referenced-by-count":126,"title":["Diversity of astroglial responses across human neurodegenerative disorders and brain aging"],"prefix":"10.1111","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9888-8754","authenticated-orcid":false,"given":"Isidro","family":"Ferrer","sequence":"first","affiliation":[{"name":"Department of Pathology and Experimental Therapeutics University of Barcelona Barcelona Spain"},{"name":"Institute of Neuropathology Pathologic Anatomy Service, Bellvitge University Hospital, IDIBELL, Hospitalet de Llobregat Barcelona 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