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- W143399520 abstract "Recent neurochemical studies in postmortem brains of patients with Parkinson's disease (PD), PD with dementia (PDD) and age-matched controls revealed significant decrease of tyrosine hydroxylase (TH) and dopamine transporter (DAT) in striatum, confirming previous studies indicating substantial loss of dopaminergic neurons and terminals. Insoluble α-synuclein (αSyn) was significantly increased in both striata and inferior frontal gyrus (IFG), more severe in PDD, probably related to Lewy body (LB) burden discussed as one cause of dementia in PD. Parkin levels frequently related to recessive and young-onset PD were unchanged, suggesting no link to sporadic PD. Novel and most interesting data showed elevated tauopathy in striata of both PD and PDD, associated with increased levels of phosphorylated GSK-3β and reduced 20S proteasomal subunits but – despite increased cortical αSyn – unchanged pTau in IFG, related to increased pGSK-3β and decreased 19S proteasome subunits. These data, recently confirmed in PDGF-αSyn transgenic mice (Haggerty et al., submitted) suggest tauopathy in PD and PDD restricted to the dopaminergic nigrostriatal system and in various animal models of PD show topographic differences from a global tauopathy in Alzheimer's disease (AD) (and other tauopathies). Although some of these data are at variance to current neuropathologic findings in PD and PDD, they confirm frequently discussed correlations/overlaps between AD and PD/PDD and synergistic effects of αSyn, pTau, β-amyloid, and other pathologic proteins, suggesting a dualism or triad of neurodegeneration, the basic molecular pathogenesis remains to be elucidated." @default.
- W143399520 created "2016-06-24" @default.
- W143399520 creator A5042083351 @default.
- W143399520 date "2011-01-01" @default.
- W143399520 modified "2023-09-25" @default.
- W143399520 title "Interaction between α-synuclein and tau in Parkinson's disease" @default.
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