Decreased platelet glutamate uptake and genetic risk factors in patients with Parkinson's disease
Abstract
Genetic risk factors seem to play a role in sporadic Parkinson's disease (PD), maybe triggering oxidative stress and excitotoxicity within substantia nigra. However, genetic factors act at systemic level: reduced activity of mitochondrial enzymes and decreased glutamate uptake have been shown in platelets from PD patients. In this study we investigated glutamate uptake in platelets from 38 sporadic PD patients, 13 patients with parkinsonian syndromes and 28 controls and assessed polymorphisms of alpha-synuclein and ApoE genes. A 48% reduction of glutamate uptake p)<0.0001) was observed in PD patients which, with respect to control groups, correlated with the disease severity (r = -0.44, p < 0.05). Genetic studies of this population did not show differences between PD and controls, nor correlations with platelet glutamate uptake.
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Glutamate in the brain is mainly cleared by GLT-1.
“Glutamate in the brain is mainly cleared by GLT-1”
From Neuroprotective Effect of Ceftriaxone on MPTP‐Induced Parkinson’s Disease Mouse Model by Regulating Inflammation and Intestinal Microbiota (2021) · cites this paper as [26]
GLT-1 shows dysfunction or decreased expression in patients with neurodegenerative diseases such as PD, AD, or ALS.
“GLT-1 shows dysfunction or decreased expression in patients with neurodegenerative diseases such as PD [26], AD [27], or ALS [17]”
From Neuroprotective Effect of Ceftriaxone on MPTP‐Induced Parkinson’s Disease Mouse Model by Regulating Inflammation and Intestinal Microbiota (2021) · cites this paper as [26]
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Glutamate uptake inhibition by oxygen free radicals in rat cortical astrocytes
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“Impaired mitochondrial function in PD are also described in peripheral tissues and in platelets [3], where we have previously reported decreased glutamate uptake, corre-”
BackgroundVariability and validity of polymorphism association studies in Parkinson’s disease
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Reduced platelet glutamate uptake in Parkinson's disease
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Zhou, X., Lu, J., Wei, K., Wei, J., Tian, P., Yue, M., Wang, Y., Hong, D., Li, F., Wang, B., et al. (2021) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2021/9424582 · Cited by 85 · see citing works
Ceftriaxone Protects Astrocytes from MPP+ via Suppression of NF-ΚB/JNK/c-Jun Signaling
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- Authors
- Ferrarese, C., Tremolizzo, L., Rigoldi, M., Sala, G., Brighina, L., Ricci, G., Albizzati, M. G., Piolti, R., Crosti, F., Dalpr�, L., Frattola, L., & Begni, B.
- Affiliations
- University of Milano-Bicocca (IT)
- Azienda Ospedaliera San Gerardo (IT)
- Venue
- Neurological Sciences
- Published
- 2001-02-01
- Volume
- 22
- Issue
- 1
- Pages
- 65-66
- ISSN
- 1590-1874 (ISSN-L)
- 1590-3478
- OpenAlex
- W1988015462
- Cited by
- 39
- References
- 8
- Citations by year
- 2025: 2 · 2023: 3 · 2022: 1 · 2021: 3 · 2020: 2 · 2019: 3 · 2018: 1 · 2017: 2 · 2016: 1 · 2014: 1
- FWCI
- 1.18
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neurological Sciences (publishedVersion)
- PubMed (publishedVersion)
- BOA (University of Milano-Bicocca) (submittedVersion)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Neurology › Neurological disorders and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- Parkinson's disease, genetic risk factors, APOE polymorphism, parkinsonism, disease severity, mitochondrial enzymes, oxidative stress, excitotoxicity, substantia nigra
- MeSH terms
- Apolipoproteins E, Blood Platelets, Brain, Energy Metabolism, Gene Frequency, Genetic Markers, Genotype, Humans, Mitochondria, Nerve Tissue Proteins, Parkinson Disease, Polymorphism, Genetic, Risk Factors, Cell Death, Oxidative Stress, Glutamic Acid, Genetic Predisposition to Disease, Synucleins, alpha-Synuclein
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