G5 Artikkeliväitöskirja
Clinical significance of nigral neuropathology in parkinsonian disorders: A comparative clinicopathological study
Tekijät: Backman, Emmilotta
Kustannuspaikka: Turku
Julkaisuvuosi: 2026
Sarjan nimi: Annales Universitatis Turkuensis D
Numero sarjassa: 1956
ISBN: 978-952-02-0588-1
eISBN: 978-952-02-0589-8
ISSN: 0355-9483
eISSN: 2343-3213
Julkaisun avoimuus kirjaamishetkellä: Avoimesti saatavilla
Julkaisukanavan avoimuus : Kokonaan avoin julkaisukanava
Verkko-osoite: https://urn.fi/URN:ISBN:978-952-02-0589-8
Tiivistelmä
Parkinson’s disease (PD) and atypical parkinsonisms are neurodegenerative disorders marked by overlapping motor symptoms such as stiffness, slow movements, and tremor, collectively termed parkinsonism. In PD, progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc) leads to striatal dopamine depletion, driving the classical motor phenotype. Non motor symptoms, including cognitive decline, mood and sleep disturbances, and autonomic dysfunction, further impair quality of life. Atypical parkinsonisms, including multiple system atrophy (MSA), and progressive supranuclear palsy (PSP), share core motor features with PD but are distinguished by faster progression, poor levodopa response, and a broader neuropathology, together with severe nigral degeneration. This thesis investigated neuroinflammation and neural density in the SNc by comparing PD with MSA and PSP. Immunohistochemial analyses, clinical features, medication, and computed tomography (CT) imaging evaluation were assessed. Brain tissue and corresponding clinical records from the University Hospital Turku (between 2002 and 2021) were examined. Tyrosine hydroxylase (TH) positive neurons were manually quantified, while neuroinflammatory cells were assessed via automated analysis. Results revealed pronounced T cell infiltration in PSP, with elevated CD3+, CD4+, and CD8+ T cell counts relative to PD, MSA, and controls, whereas microglial activity was most pronounced in PD. Levodopa was not associated with neurotoxicity or inflammation. Moreover, depressed PD patients exhibited more severe cortical atrophy than non-depressed counterparts. These findings support existing evidence of distinct inflammatory and neuronal signatures across the disorders, suggesting potential disease-specific mechanisms and therapeutic targets. Moreover, depression, a common non-motor symptom in PD, appears to be associated with cortical atrophy, while levodopa, the golden standard medical treatment for parkinsonian syndromes, does not affect nigral neuronal survival or neuroinflammatory activity in PD, PSP, or MSA.
Parkinson’s disease (PD) and atypical parkinsonisms are neurodegenerative disorders marked by overlapping motor symptoms such as stiffness, slow movements, and tremor, collectively termed parkinsonism. In PD, progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc) leads to striatal dopamine depletion, driving the classical motor phenotype. Non motor symptoms, including cognitive decline, mood and sleep disturbances, and autonomic dysfunction, further impair quality of life. Atypical parkinsonisms, including multiple system atrophy (MSA), and progressive supranuclear palsy (PSP), share core motor features with PD but are distinguished by faster progression, poor levodopa response, and a broader neuropathology, together with severe nigral degeneration. This thesis investigated neuroinflammation and neural density in the SNc by comparing PD with MSA and PSP. Immunohistochemial analyses, clinical features, medication, and computed tomography (CT) imaging evaluation were assessed. Brain tissue and corresponding clinical records from the University Hospital Turku (between 2002 and 2021) were examined. Tyrosine hydroxylase (TH) positive neurons were manually quantified, while neuroinflammatory cells were assessed via automated analysis. Results revealed pronounced T cell infiltration in PSP, with elevated CD3+, CD4+, and CD8+ T cell counts relative to PD, MSA, and controls, whereas microglial activity was most pronounced in PD. Levodopa was not associated with neurotoxicity or inflammation. Moreover, depressed PD patients exhibited more severe cortical atrophy than non-depressed counterparts. These findings support existing evidence of distinct inflammatory and neuronal signatures across the disorders, suggesting potential disease-specific mechanisms and therapeutic targets. Moreover, depression, a common non-motor symptom in PD, appears to be associated with cortical atrophy, while levodopa, the golden standard medical treatment for parkinsonian syndromes, does not affect nigral neuronal survival or neuroinflammatory activity in PD, PSP, or MSA.
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