Review Article
Will Posttranslational Modifications of Brain Proteins Provide Novel Serological Markers for Dementias?
Table 4
Proteins, proteases, and the consequences in relation to dementia.
| Protein | Normal function | Protease | Alteration and consequence | Disease | Reference |
| APP | Lipid metabolism, axonal transport?? | α,β,γ-Secretases ADAMs MMPs | Fragmentation, generation of Aβ, formation of amyloid plaques | AD | [28, 94, 95] | tau | Microtubule stabilizing protein | Caspase Calpain | C-terminal truncation in AD and aggregation causing NFTs | AD | [28, 73–75] | α-Synuclein | Molecular chaperone | MMPs calpain cathepsins | Truncation and aggregation leading to Lewy bodies | DLB | [34, 35, 96, 97] | TDP-43 | Transcription and splicing regulation, apoptosis, cell division, and stabilisation of messenger RNA | Caspase? | C-terminal truncation, aggregation formation of Lewy bodies | FTLD-TDPAD | [37, 39, 98, 99] | FUS | Transcription factor | ?? | ?? | FTLD-FUS | [39] | GFAP | Neurofilament | Caspase | Truncation and neuronal death | Alexander disease | [100] |
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