<unk>  can be explained as cell loss and gliosis or a proliferation of astrocytes in damaged areas of the central nervous<unk> . This damage forms a scar which is then termed a glial scar. The presence of inclusion bodies known as Papp–Lantos bodies, in the movement, balance, and autonomic-control centres of the brain are the defining histopathologic hallmark of<unk> . The major filamentous component of Papp-Lantos bodies, glial and neuronal cytoplasmic inclusions, is alpha-synuclein. Mutations in this substance may play a role in the disease. The conformation of the alpha-synuclein is different from that of alpha-synuclein in Lewy bodies. The disease probably starts with an oligodendrogliopathy. Tau proteins have been found in some glial cytoplasmic inclusion bodies.
Multiple system atrophy
Pure autonomic failure
Progressive supranuclear palsy
Tropical ataxic neuropathy
Low pressure hydrocephalus
Spinal and bulbar muscular atrophy
Lewy body dementias
Amyotrophic lateral sclerosis