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Article: APOE

Costa-Laparra, Irene / Juárez-Escoto, Elena / Vicario, Carlos / Moratalla, Rosario / García-Sanz, Patricia

2023 Volume 15, Page(s) 1087072

Abstract: Introduction: Alzheimer's disease remains the most common neurodegenerative disorder, depicted mainly by memory loss and the presence in the brain of senile plaques and neurofibrillary tangles. This disease is related to several cellular alterations ... ...

Abstract	Introduction: Alzheimer's disease remains the most common neurodegenerative disorder, depicted mainly by memory loss and the presence in the brain of senile plaques and neurofibrillary tangles. This disease is related to several cellular alterations like the loss of synapses, neuronal death, disruption of lipid homeostasis, mitochondrial fragmentation, or raised oxidative stress. Notably, changes in the autophagic pathway have turned out to be a key factor in the early development of the disease. The aim of this research is to determine the impact of the Methods: Fibroblasts from Alzheimer's patients with Results: We observed that the Conclusion: The findings suggest that all these modifications could eventually contribute to the neuronal degeneration that underlies the pathogenesis of Alzheimer's disease. Further research in this area may help to develop targeted therapies for the treatment of Alzheimer's disease.
Language	English
Publishing date	2023-06-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2023.1087072
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Article ; Online: The importance of cholesterol in Parkinson's disease.

García-Sanz, Patricia / Moratalla, Rosario

Movement disorders : official journal of the Movement Disorder Society

2018 Volume 33, Issue 2, Page(s) 343–344

MeSH term(s)	Animals ; Cholesterol ; Endoplasmic Reticulum ; Lipid Droplets ; Lysosomes ; Parkinson Disease
Chemical Substances	Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2018-01-09
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	607633-6
ISSN	1531-8257 ; 0885-3185
ISSN (online)	1531-8257
ISSN	0885-3185
DOI	10.1002/mds.27251
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Article ; Online: An innovative framework to determine the implementation level of personalized medicine: A systematic review.

Aguilera-Cobos, Lorena / García-Sanz, Patricia / Rosario-Lozano, María Piedad / Claros, M Gonzalo / Blasco-Amaro, Juan Antonio

Frontiers in public health

2023 Volume 11, Page(s) 1039688

Abstract: Background: Personalized medicine (PM) is now the new frontier in patient care. The application of this new paradigm extends to various pathologies and different patient care phases, such as diagnosis and treatment. Translating biotechnological advances ...

Abstract	Background: Personalized medicine (PM) is now the new frontier in patient care. The application of this new paradigm extends to various pathologies and different patient care phases, such as diagnosis and treatment. Translating biotechnological advances to clinical routine means adapting health services at all levels is necessary. Purpose: This article aims to identify the elements for devising a framework that will allow the level of PM implementation in the country under study to be quantitatively and qualitatively assessed and that can be used as a guideline for future implementation plans. Methods: A systematic review was conducted per Results: 19 full-text studies that met the inclusion criteria were peer-selected in the systematic review. From all the studies that were included, 37 elements-encompassed in 11 domains-were extracted for determining the degree of PM implementation. These domains and their constituent elements comprise the qualitative and quantitative assessment framework presented herein. Each of the elements can be assessed individually. On the other hand, the domains were standardized to all have the same weight in an overall assessment. Conclusions: A framework has been developed that takes a multi-factorial approach to determine the degree of implementation of PM at the national level. This framework could also be used to rank countries and their implementation strategies according to the score they receive in the application of the latter. It could also be used as a guide for developing future national PM implementation strategies. Systematic review registration: https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42022338611, Identifier: CRD42022338611.
MeSH term(s)	Humans ; Precision Medicine ; Biotechnology ; Peer Group
Language	English
Publishing date	2023-02-03
Publishing country	Switzerland
Document type	Systematic Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2711781-9
ISSN	2296-2565 ; 2296-2565
ISSN (online)	2296-2565
ISSN	2296-2565
DOI	10.3389/fpubh.2023.1039688
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Article ; Online: The Role of Cholesterol in α-Synuclein and Lewy Body Pathology in GBA1 Parkinson's Disease.

García-Sanz, Patricia / M F G Aerts, Johannes / Moratalla, Rosario

Movement disorders : official journal of the Movement Disorder Society

2020 Volume 36, Issue 5, Page(s) 1070–1085

Abstract: Parkinson's disease (PD) is a progressive neurodegenerative disease where dopaminergic neurons in the substantia nigra are lost, resulting in a decrease in striatal dopamine and, consequently, motor control. Dopaminergic degeneration is associated with ... ...

Abstract	Parkinson's disease (PD) is a progressive neurodegenerative disease where dopaminergic neurons in the substantia nigra are lost, resulting in a decrease in striatal dopamine and, consequently, motor control. Dopaminergic degeneration is associated with the appearance of Lewy bodies, which contain membrane structures and proteins, including α-synuclein (α-Syn), in surviving neurons. PD displays a multifactorial pathology and develops from interactions between multiple elements, such as age, environmental conditions, and genetics. Mutations in the GBA1 gene represent one of the major genetic risk factors for PD. This gene encodes an essential lysosomal enzyme called β-glucocerebrosidase (GCase), which is responsible for degrading the glycolipid glucocerebroside into glucose and ceramide. GCase can generate glucosylated cholesterol via transglucosylation and can also degrade the sterol glucoside. Although the molecular mechanisms that predispose an individual to neurodegeneration remain unknown, the role of cholesterol in PD pathology deserves consideration. Disturbed cellular cholesterol metabolism, as reflected by accumulation of lysosomal cholesterol in GBA1-associated PD cellular models, could contribute to changes in lipid rafts, which are necessary for synaptic localization and vesicle cycling and modulation of synaptic integrity. α-Syn has been implicated in the regulation of neuronal cholesterol, and cholesterol facilitates interactions between α-Syn oligomers. In this review, we integrate the results of previous studies and describe the cholesterol landscape in cellular homeostasis and neuronal function. We discuss its implication in α-Syn and Lewy body pathophysiological mechanisms underlying PD, focusing on the role of GCase and cholesterol. © 2020 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
MeSH term(s)	Cholesterol ; Glucosylceramidase/genetics ; Humans ; Lewy Bodies ; Neurodegenerative Diseases ; Parkinson Disease/genetics ; alpha-Synuclein/genetics
Chemical Substances	alpha-Synuclein ; Cholesterol (97C5T2UQ7J) ; Glucosylceramidase (EC 3.2.1.45)
Language	English
Publishing date	2020-11-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	607633-6
ISSN	1531-8257 ; 0885-3185
ISSN (online)	1531-8257
ISSN	0885-3185
DOI	10.1002/mds.28396
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Article: Modeling Parkinson's Disease With the Alpha-Synuclein Protein.

Gómez-Benito, Mónica / Granado, Noelia / García-Sanz, Patricia / Michel, Anne / Dumoulin, Mireille / Moratalla, Rosario

Frontiers in pharmacology

2020 Volume 11, Page(s) 356

Abstract: Alpha-synuclein (α-Syn) is a key protein involved in Parkinson's disease (PD) pathology. PD is characterized by the loss of dopaminergic neuronal cells in the substantia nigra pars compacta and the abnormal accumulation and aggregation of α-Syn in the ... ...

Abstract	Alpha-synuclein (α-Syn) is a key protein involved in Parkinson's disease (PD) pathology. PD is characterized by the loss of dopaminergic neuronal cells in the substantia nigra pars compacta and the abnormal accumulation and aggregation of α-Syn in the form of Lewy bodies and Lewy neurites. More precisely, the aggregation of α-Syn is associated with the dysfunctionality and degeneration of neurons in PD. Moreover, mutations in the Significance: Here, we show that injection of α-Syn PFFs and overexpression of α-Syn mediated by rAAV lead to a different pattern of PD pathology in rodents. First, α-Syn PFFs models trigger the Lewy body-like inclusions formation in brain regions directly interconnected with the injection site, suggesting that there is an inter-neuronal transmission of the α-Syn pathology. In contrast, rAAV-mediated α-Syn overexpression in the brain limits the α-Syn aggregates within the transduced neurons. Second, phosphorylated α-Syn inclusions obtained with rAAV are predominantly nuclear with a punctate appearance that becomes diffuse along the neuronal fibers, whereas α-Syn PFFs models lead to the formation of cytoplasmic aggregates of phosphorylated α-Syn reminiscent of Lewy bodies and Lewy neurites.
Language	English
Publishing date	2020-04-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2020.00356
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Article ; Online: Embryonic defence mechanisms against glucose-dependent oxidative stress require enhanced expression of Alx3 to prevent malformations during diabetic pregnancy.

García-Sanz, Patricia / Mirasierra, Mercedes / Moratalla, Rosario / Vallejo, Mario

Scientific reports

2017 Volume 7, Issue 1, Page(s) 389

Abstract: Oxidative stress constitutes a major cause for increased risk of congenital malformations associated to severe hyperglycaemia during pregnancy. Mutations in the gene encoding the transcription factor ALX3 cause congenital craniofacial and neural tube ... ...

Abstract	Oxidative stress constitutes a major cause for increased risk of congenital malformations associated to severe hyperglycaemia during pregnancy. Mutations in the gene encoding the transcription factor ALX3 cause congenital craniofacial and neural tube defects. Since oxidative stress and lack of ALX3 favour excessive embryonic apoptosis, we investigated whether ALX3-deficiency further increases the risk of embryonic damage during gestational hyperglycaemia in mice. We found that congenital malformations associated to ALX3-deficiency are enhanced in diabetic pregnancies. Increased expression of genes encoding oxidative stress-scavenging enzymes in embryos from diabetic mothers was blunted in the absence of ALX3, leading to increased oxidative stress. Levels of ALX3 increased in response to glucose, but ALX3 did not activate oxidative stress defence genes directly. Instead, ALX3 stimulated the transcription of Foxo1, a master regulator of oxidative stress-scavenging genes, by binding to a newly identified binding site located in the Foxo1 promoter. Our data identify ALX3 as an important component of the defence mechanisms against the occurrence of developmental malformations during diabetic gestations, stimulating the expression of oxidative stress-scavenging genes in a glucose-dependent manner via Foxo1 activation. Thus, ALX3 deficiency provides a novel molecular mechanism for developmental defects arising from maternal hyperglycaemia.
MeSH term(s)	Animals ; Embryo, Mammalian/metabolism ; Embryo, Mammalian/pathology ; Embryonic Development ; Female ; Gene Expression Regulation, Developmental ; Glucose/administration & dosage ; Glucose/metabolism ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Hyperglycemia/complications ; Hyperglycemia/genetics ; Hyperglycemia/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Oxidative Stress ; Pregnancy ; Pregnancy in Diabetics/genetics ; Pregnancy in Diabetics/metabolism
Chemical Substances	Alx3 protein, mouse ; Homeodomain Proteins ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2017-03-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-00334-1
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Article ; Online: Cholesterol and multilamellar bodies: Lysosomal dysfunction in GBA-Parkinson disease.

García-Sanz, Patricia / Orgaz, Lorena / Fuentes, José M / Vicario, Carlos / Moratalla, Rosario

Autophagy

2018 Volume 14, Issue 4, Page(s) 717–718

Abstract: Lipid and cholesterol metabolism might play a role in the pathogenesis of Parkinson disease (PD). However, the association between cholesterol and PD is not clearly established. Cholesterol accumulation is closely related to the expression of ... ...

Abstract	Lipid and cholesterol metabolism might play a role in the pathogenesis of Parkinson disease (PD). However, the association between cholesterol and PD is not clearly established. Cholesterol accumulation is closely related to the expression of multilamellar bodies (MLBs). Also, cholesterol controls autophagosome transport. Thus, impaired cholesterol and autophagosome trafficking might lead to robust autophagic vacuole accumulation. Our recent work provides the first evidence that the presence of the N370S GBA mutation produces an accumulation of cholesterol, which alters autophagy-lysosome function with the appearance of MLBs, rendering the cell more vulnerable and sensitive to apoptosis.
MeSH term(s)	Autophagosomes/metabolism ; Autophagy/genetics ; Cholesterol/metabolism ; Glucosylceramidase/metabolism ; Humans ; Lipid Metabolism/genetics ; Lysosomes/genetics ; Lysosomes/metabolism ; Mutation/genetics ; Parkinson Disease/genetics ; Parkinson Disease/pathology
Chemical Substances	Cholesterol (97C5T2UQ7J) ; Glucosylceramidase (EC 3.2.1.45)
Language	English
Publishing date	2018-03-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2018.1427396
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Article ; Online: Differential configurations involving binding of USF transcription factors and Twist1 regulate Alx3 promoter activity in mesenchymal and pancreatic cells.

García-Sanz, Patricia / Fernández-Pérez, Antonio / Vallejo, Mario

The Biochemical journal

2013 Volume 450, Issue 1, Page(s) 199–208

Abstract: During embryonic development, the aristaless-type homeodomain protein Alx3 is expressed in the forehead mesenchyme and contributes to the regulation of craniofacial development. In the adult, Alx3 is expressed in pancreatic islets where it participates ... ...

Abstract	During embryonic development, the aristaless-type homeodomain protein Alx3 is expressed in the forehead mesenchyme and contributes to the regulation of craniofacial development. In the adult, Alx3 is expressed in pancreatic islets where it participates in the control of glucose homoeostasis. In the present study, we investigated the transcriptional regulation of Alx3 gene expression in these two cell types. We found that the Alx3 promoter contains two E-box regulatory elements, named EB1 and EB2, that provide binding sites for the basic helix-loop-helix transcription factors Twist1, E47, USF (upstream stimulatory factor) 1 and USF2. In primary mouse embryonic mesenchymal cells isolated from the forehead, EB2 is bound by Twist1, whereas EB1 is bound by USF1 and USF2. Integrity of both EB1 and EB2 is required for Twist1-mediated transactivation of the Alx3 promoter, even though Twist1 does not bind to EB1, indicating that binding of USF1 and USF2 to this element is required for Twist1-dependent Alx3 promoter activity. In contrast, in pancreatic islet insulin-producing cells, the integrity of EB2 is not required for proximal promoter activity. The results of the present study indicate that USF1 and USF2 are important regulatory factors for Alx3 gene expression in different cell types, whereas Twist1 contributes to transcriptional transactivation in mesenchymal, but not in pancreatic, cells.
MeSH term(s)	Animals ; Binding Sites ; COS Cells ; Cell Line ; Cercopithecus aethiops ; Embryo, Mammalian/metabolism ; Female ; Glucagon-Secreting Cells/metabolism ; HeLa Cells ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Humans ; Mesoderm/metabolism ; Mice ; NIH 3T3 Cells ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Pregnancy ; Promoter Regions, Genetic ; Twist-Related Protein 1/genetics ; Twist-Related Protein 1/metabolism ; Upstream Stimulatory Factors/genetics ; Upstream Stimulatory Factors/metabolism
Chemical Substances	Alx3 protein, mouse ; Homeodomain Proteins ; Nuclear Proteins ; Twist-Related Protein 1 ; USF1 protein, human ; Upstream Stimulatory Factors ; Usf2 protein, mouse ; Twist1 protein, mouse (136253-27-5)
Language	English
Publishing date	2013-02-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2969-5
ISSN	1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
ISSN (online)	1470-8728
ISSN	0006-2936 ; 0306-3275 ; 0264-6021
DOI	10.1042/BJ20120962
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Article ; Online: L-DOPA Reverses the Increased Free Amino Acids Tissue Levels Induced by Dopamine Depletion and Rises GABA and Tyrosine in the Striatum.

Solís, Oscar / García-Sanz, Patricia / Herranz, Antonio S / Asensio, María-José / Moratalla, Rosario

Neurotoxicity research

2016 Volume 30, Issue 1, Page(s) 67–75

Abstract: Perturbations in the cerebral levels of various amino acids are associated with neurological disorders, and previous studies have suggested that such alterations have a role in the motor and non-motor symptoms of Parkinson's disease. However, the direct ... ...

Abstract	Perturbations in the cerebral levels of various amino acids are associated with neurological disorders, and previous studies have suggested that such alterations have a role in the motor and non-motor symptoms of Parkinson's disease. However, the direct effects of chronic L-DOPA treatment, that produces dyskinesia, on neural tissue amino acid concentrations have not been explored in detail. To evaluate whether striatal amino acid concentrations are altered in peak dose dyskinesia, 6-hydroxydopamine (6-OHDA)-lesioned hemiparkinsonian mice were treated chronically with L-DOPA and tissue amino acid concentrations were assessed by HPLC analysis. These experiments revealed that neither 6-OHDA nor L-DOPA treatment are able to alter glutamate in the striatum. However, glutamine increases after 6-OHDA and returns back to normal levels with L-DOPA treatment, suggesting increased striatal glutamatergic transmission with lack of dopamine. In addition, glycine and taurine levels are increased following dopamine denervation and restored to normal levels by L-DOPA. Interestingly, dyskinetic animals showed increased levels of GABA and tyrosine, while aspartate striatal tissue levels are not altered. Overall, our results indicate that chronic L-DOPA treatment, besides normalizing the altered levels of some amino acids after 6-OHDA, robustly increases striatal GABA and tyrosine levels which may in turn contribute to the development of L-DOPA-induced dyskinesia.
MeSH term(s)	Amino Acids/metabolism ; Animals ; Aspartic Acid/metabolism ; Corpus Striatum/drug effects ; Corpus Striatum/metabolism ; Dopamine/deficiency ; Dyskinesia, Drug-Induced/metabolism ; Forelimb/drug effects ; Glutamic Acid/metabolism ; Glycine/metabolism ; Levodopa/pharmacology ; Mice ; Oxidopamine/metabolism ; Rotarod Performance Test ; Taurine/metabolism ; Tyrosine/metabolism ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	Amino Acids ; Taurine (1EQV5MLY3D) ; Aspartic Acid (30KYC7MIAI) ; Glutamic Acid (3KX376GY7L) ; Tyrosine (42HK56048U) ; Levodopa (46627O600J) ; gamma-Aminobutyric Acid (56-12-2) ; Oxidopamine (8HW4YBZ748) ; Glycine (TE7660XO1C) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2016-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2036826-4
ISSN	1476-3524 ; 1029-8428
ISSN (online)	1476-3524
ISSN	1029-8428
DOI	10.1007/s12640-016-9612-x
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Article ; Online: Dopamine D2R is Required for Hippocampal-dependent Memory and Plasticity at the CA3-CA1 Synapse.

Espadas, Isabel / Ortiz, Oscar / García-Sanz, Patricia / Sanz-Magro, Adrián / Alberquilla, Samuel / Solis, Oscar / Delgado-García, José María / Gruart, Agnès / Moratalla, Rosario

Cerebral cortex (New York, N.Y. : 1991)

2020 Volume 31, Issue 4, Page(s) 2187–2204

Abstract: Dopamine receptors play an important role in motivational, emotional, and motor responses. In addition, growing evidence suggests a key role of hippocampal dopamine receptors in learning and memory. It is well known that associative learning and synaptic ...

Abstract	Dopamine receptors play an important role in motivational, emotional, and motor responses. In addition, growing evidence suggests a key role of hippocampal dopamine receptors in learning and memory. It is well known that associative learning and synaptic plasticity of CA3-CA1 requires the dopamine D1 receptor (D1R). However, the specific role of the dopamine D2 receptor (D2R) on memory-related neuroplasticity processes is still undefined. Here, by using two models of D2R loss, D2R knockout mice (Drd2-/-) and mice with intrahippocampal injections of Drd2-small interfering RNA (Drd2-siRNA), we aimed to investigate how D2R is involved in learning and memory as well as in long-term potentiation of the hippocampus. Our studies revealed that the genetic inactivation of D2R impaired the spatial memory, associative learning, and the classical conditioning of eyelid responses. Similarly, deletion of D2R reduced the activity-dependent synaptic plasticity in the hippocampal CA1-CA3 synapse. Our results demonstrate the first direct evidence that D2R is essential in behaving mice for trace eye blink conditioning and associated changes in hippocampal synaptic strength. Taken together, these results indicate a key role of D2R in regulating hippocampal plasticity changes and, in consequence, acquisition and consolidation of spatial and associative forms of memory.
MeSH term(s)	Animals ; Avoidance Learning/physiology ; CA1 Region, Hippocampal/metabolism ; CA3 Region, Hippocampal/metabolism ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neuronal Plasticity/physiology ; RNA, Small Interfering/administration & dosage ; Receptors, Dopamine D2/deficiency ; Receptors, Dopamine D2/genetics ; Spatial Memory/physiology ; Synapses/genetics ; Synapses/metabolism
Chemical Substances	RNA, Small Interfering ; Receptors, Dopamine D2
Language	English
Publishing date	2020-11-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1077450-6
ISSN	1460-2199 ; 1047-3211
ISSN (online)	1460-2199
ISSN	1047-3211
DOI	10.1093/cercor/bhaa354
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