Cerebrospinal fluid markers analysis in the differential diagnosis of dementia with Lewy bodies and Parkinson’s disease dementia

Gmitterová, Karin; Gawinecka, Joanna; Llorens, Franc; Varges, Daniela; Valkovič, Peter; Zerr, Inga

doi:10.1007/s00406-018-0928-9

Cited by 19 publications

(20 citation statements)

References 61 publications

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“…We observed increased levels of GFAP, S100B and MBP, but not of NSE, in CSF of PD in comparison to controls. These results are partly in agreement with previous studies, showing no differences in S100B and NSE levels in serum [21] and in CSF [22] between PD and controls. Yet, other studies reported no significant differences in CSF GFAP levels between PD and controls [9,23].…”

Section: Discussionsupporting

confidence: 93%

“…Several studies have reported increased levels of the glial proteins S100B and GFAP in CSF and in serum of patients with dementia, i.e. AD, FTD and dementia with Lewy bodies (DLB) [9,10,22,[25][26][27]. The higher levels in CSF and serum of GFAP and S100B in dementia might indicate an association between glial proteins and cognitive functioning, since S100B levels in CSF [26,28] and in serum [29], and of GFAP in serum [9] and CSF [27] correlated with the severity of cognitive dysfunction in AD patients.…”

Section: Discussionmentioning

confidence: 99%

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Cerebrospinal fluid myelin basic protein is elevated in multiple system atrophy

Santaella

Kuiperij

Rumund³

et al. 2020

Parkinsonism & Related Disorders

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Introduction: Parkinson's disease (PD) and multiple system atrophy (MSA) have overlapping symptoms, challenging an early diagnosis. Diagnostic accuracy is important because PD and MSA have a different prognosis and response to treatment. Here, we aimed to evaluate the diagnostic value of brain-specific structural proteins in cerebrospinal fluid (CSF) of PD and MSA patients, as well as their association with cognitive decline. Methods: CSF samples were collected from patients with clear signs of parkinsonism, but with uncertain diagnosis at the time of inclusion. Clinical diagnoses of PD (n = 55) and MSA (n = 22) were established after 3 and 10 years of follow-up and re-evaluated after 12 years, according to the most updated clinical criteria. CSF from controls (n = 118) was studied for comparison. Neuron-specific enolase (NSE), glial fibrillary acidic protein (GFAP), S100 calcium-binding protein B (S100B) and myelin basic protein (MBP) levels in CSF were measured using ELISA. Protein levels were also correlated with cognitive decline, i.e. worsening of the mini mental state examination (MMSE) over a period of three years. Results: MBP concentrations were increased in MSA compared to PD and controls (p < 0.005) and could differentiate MSA and PD with high accuracy (AUC = 0.781; p < 0.001). Concentrations of MPB, GFAP and S100B, but not NSE, were significantly elevated in PD patients compared to controls (p = 0.05). None of the brain-specific structural proteins correlated with MMSE progression. Conclusions: Our results demonstrate that MBP differentiates PD from MSA at early stages of the disease, indicating that demyelination and axonal damage may already occur in early stages of MSA.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Cerebrospinal fluid myelin basic protein is elevated in multiple system atrophy

Santaella

Kuiperij

Rumund³

et al. 2020

Parkinsonism & Related Disorders

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“…Severity of dementia associated with CSF tau and p‐tau levels in DLB and CSF tau and p‐tau ratio in PDD. Also, rapid disease course was associated with the decrease of Aβ 1‐42 in DLB . Significantly lower levels of CSF Aβ 1‐42 was found in neuropathologically confirmed DLB cases with Aβ plaques compared to DLB without Aβ plaques .…”

Section: Methodsmentioning

confidence: 86%

Review: Clinical, neuropathological and genetic features of Lewy body dementias

Hansen

Ling

Lashley

et al. 2019

Neuropathology Appl Neurobio

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2019) Neuropathology and Applied Neurobiology 45, 635-654 Clinical, neuropathological and genetic features of Lewy body dementias Lewy body dementias are the second most common neurodegenerative dementias after Alzheimer's disease and include dementia with Lewy bodies and Parkinson's disease dementia. They share similar clinical and neuropathological features but differ in the time of dementia and parkinsonism onset. Although Lewy bodies are their main pathological hallmark, several studies have shown the emerging importance of Alzheimer's disease pathology. Clinical amyloid-b imaging using Pittsburgh Compound B (PiB) supports neuropathological studies which found that amyloid-b pathology is more common in dementia with Lewy bodies than in Parkinson's disease dementia. Nevertheless, other co-occurring pathologies, such as cerebral amyloid angiopathy, TDP-43 pathology and synaptic pathology may also influence the development of neurodegeneration and dementia. Recent genetic studies demonstrated an important role of APOE genotype and other genes such as GBA and SNCA which seem to be involved in the pathophysiology of Lewy body dementias. The aim of this article is to review the main clinical, neuropathological and genetic aspects of dementia with Lewy bodies and Parkinson's disease dementia. This is particularly relevant as future management for these two conditions may differ.

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“…The sustained microglial activation in PD appears likely to reflect DAMP-mediated activation of certain toll-like receptors (notably TLR2 and TLR4), as well as the receptor of advanced glycation end-products (RAGE), the integrin receptor Mac1, and CD11b [25][26][27][28][29][30][31][32][33][34][35]. Rodent and cell culture studies suggest that HMGB1 (which activates TLR4, RAGE, and Mac1), S100B (primarily of astrocyte origin, also a RAGE ligand), and oligomeric ASYN (a ligand for TLR2 and CD11b) contribute to chronic microglial activation in PD [31,[34][35][36][37][38][39][40][41][42][43]. S100A8, S100A9, and S100A12 also have the potential to activate RAGE in this disorder; RAGE is highly promiscuous in its response to ligands [14,31,[34][35][36][37][38][39][40][41][42][43][44].…”

Section: Targeting Nadph Oxidase-phycocyanobilin/phycocyanin/spirulinamentioning

confidence: 99%

“…Rodent and cell culture studies suggest that HMGB1 (which activates TLR4, RAGE, and Mac1), S100B (primarily of astrocyte origin, also a RAGE ligand), and oligomeric ASYN (a ligand for TLR2 and CD11b) contribute to chronic microglial activation in PD [31,[34][35][36][37][38][39][40][41][42][43]. S100A8, S100A9, and S100A12 also have the potential to activate RAGE in this disorder; RAGE is highly promiscuous in its response to ligands [14,31,[34][35][36][37][38][39][40][41][42][43][44].…”

Section: Targeting Nadph Oxidase-phycocyanobilin/phycocyanin/spirulinamentioning

confidence: 99%

Nutraceuticals Targeting Generation and Oxidant Activity of Peroxynitrite May Aid Prevention and Control of Parkinson’s Disease

McCarty

Lerner

2020

IJMS

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Parkinson’s disease (PD) is a chronic low-grade inflammatory process in which activated microglia generate cytotoxic factors—most prominently peroxynitrite—which induce the death and dysfunction of neighboring dopaminergic neurons. Dying neurons then release damage-associated molecular pattern proteins such as high mobility group box 1 which act on microglia via a range of receptors to amplify microglial activation. Since peroxynitrite is a key mediator in this process, it is proposed that nutraceutical measures which either suppress microglial production of peroxynitrite, or which promote the scavenging of peroxynitrite-derived oxidants, should have value for the prevention and control of PD. Peroxynitrite production can be quelled by suppressing activation of microglial NADPH oxidase—the source of its precursor superoxide—or by down-regulating the signaling pathways that promote microglial expression of inducible nitric oxide synthase (iNOS). Phycocyanobilin of spirulina, ferulic acid, long-chain omega-3 fatty acids, good vitamin D status, promotion of hydrogen sulfide production with taurine and N-acetylcysteine, caffeine, epigallocatechin-gallate, butyrogenic dietary fiber, and probiotics may have potential for blunting microglial iNOS induction. Scavenging of peroxynitrite-derived radicals may be amplified with supplemental zinc or inosine. Astaxanthin has potential for protecting the mitochondrial respiratory chain from peroxynitrite and environmental mitochondrial toxins. Healthful programs of nutraceutical supplementation may prove to be useful and feasible in the primary prevention or slow progression of pre-existing PD. Since damage to the mitochondria in dopaminergic neurons by environmental toxins is suspected to play a role in triggering the self-sustaining inflammation that drives PD pathogenesis, there is also reason to suspect that plant-based diets of modest protein content, and possibly a corn-rich diet high in spermidine, might provide protection from PD by boosting protective mitophagy and thereby aiding efficient mitochondrial function. Low-protein diets can also promote a more even response to levodopa therapy.

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Cerebrospinal fluid markers analysis in the differential diagnosis of dementia with Lewy bodies and Parkinson’s disease dementia

Cited by 19 publications

References 61 publications

Cerebrospinal fluid myelin basic protein is elevated in multiple system atrophy

Cerebrospinal fluid myelin basic protein is elevated in multiple system atrophy

Review: Clinical, neuropathological and genetic features of Lewy body dementias

Nutraceuticals Targeting Generation and Oxidant Activity of Peroxynitrite May Aid Prevention and Control of Parkinson’s Disease

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