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Table 3 BSC studies models of proteopathic inclusion pathologies beyond Aβ and tau

From: Organotypic brain slice cultures to model neurodegenerative proteinopathies

Human PathologySlice Culture PathologyReference(s)
α-synuclein inclusionsrAAV expression of WT or A53T human α-synuclein in BSCs induces pser129 α-synuclein inclusions. rAAV expression of A53T human α-synuclein in nigrostriatal circuit BSCs also develop α-synuclein inclusions.[29, 82]
SOD-1 inclusionsSOD-1 accumulation in spinal cord slice cultures from transgenic G93A SOD-1 mice from 3 weeks in culture. SOD-1 inclusions also inducible in G85R SOD-1 transgenic spinal cord cultures with human SOD-1 seeds from spinal tissues progressively over a 20 day incubation.[85, 86]
TDP-43 inclusionsBSCs from rats expressing human mutant TDP-43 develop TDP-43 inclusions and associated micro- and astrogliosis from 10 DIV.[87]
Huntingtin inclusionsBiolistic transfection of human wild-type and mutant huntingtin (HTT) in striatal and cortical rat BSCs results in the development of HTT inclusions by 7 DIV.[89]