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Article ; Online: Vitamin D Receptor Polymorphisms in a Spanish Cohort of Parkinson's Disease Patients.

Canales-Cortés, Saray / Rodríguez-Arribas, Mario / Galindo, María F / Jordan, Joaquín / Casado-Naranjo, Ignacio / Fuentes, José M / Yakhine-Diop, Sokhna M S

Genetic testing and molecular biomarkers

2024 Volume 28, Issue 2, Page(s) 59–64

Abstract: Background: ...

Abstract	Background:
MeSH term(s)	Humans ; Case-Control Studies ; Genetic Predisposition to Disease/genetics ; Genotype ; Imidoesters ; Parkinson Disease/genetics ; Polymorphism, Single Nucleotide/genetics ; Receptors, Calcitriol/genetics ; Vitamin D
Chemical Substances	Imidoesters ; methyl 4-azidophenylacetimidate (73710-32-4) ; Receptors, Calcitriol ; Vitamin D (1406-16-2) ; VDR protein, human
Language	English
Publishing date	2024-02-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2486664-7
ISSN	1945-0257 ; 1945-0265
ISSN (online)	1945-0257
ISSN	1945-0265
DOI	10.1089/gtmb.2023.0344
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Zs.A 5195: Show issues

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Article ; Online: Comparative Genetic Analysis of the Promoters of the ATG16L1 and ATG5 Genes Associated with Sporadic Parkinson's Disease.

Gómez-Martín, Ana / Fuentes, José M / Jordán, Joaquín / Galindo, María F / Fernández-García, José Luis

Genes

2023 Volume 14, Issue 12

Abstract: Sporadic Parkinson's disease, characterised by a decline in dopamine, usually manifests in people over 65 years of age. Although 10% of cases have a genetic (familial) basis, most PD is sporadic. Genome sequencing studies have associated several genetic ... ...

Abstract	Sporadic Parkinson's disease, characterised by a decline in dopamine, usually manifests in people over 65 years of age. Although 10% of cases have a genetic (familial) basis, most PD is sporadic. Genome sequencing studies have associated several genetic variants with sporadic PD. Our aim was to analyse the promoter region of the ATG16L1 and ATG5 genes in sporadic PD patients and ethnically matched controls. Genotypes were obtained by using the Sanger method with primers designed by us. The number of haplotypes was estimated with DnaSP software, phylogeny was reconstructed in Network, and genetic divergence was explored with
MeSH term(s)	Humans ; Autophagy-Related Protein 5/genetics ; Autophagy-Related Proteins/genetics ; Genetic Predisposition to Disease ; Genotype ; Haplotypes ; Parkinson Disease/genetics ; Promoter Regions, Genetic
Chemical Substances	ATG16L1 protein, human ; ATG5 protein, human ; Autophagy-Related Protein 5 ; Autophagy-Related Proteins
Language	English
Publishing date	2023-12-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes14122171
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Article ; Online: A bibliometric evaluation of the top 100 cited natalizumab articles.

García-Fernández, Francisco Javier / García-Fernández, Alba Estela / Nava, Eduardo / Del Pozo, Julian Solis Garcia / Ikuta, Ichiro / Jordan, Joaquin / Galindo, Maria F

Journal of neuroimmunology

2020 Volume 349, Page(s) 577379

Abstract: Natalizumab is being used in recurrent multiple sclerosis despite its history of market withdrawal due to lethal cases. We have carried out a bibliometric analysis of this drug from 1999 to February 2020 in order to assess the real impact of the use ... ...

Abstract	Natalizumab is being used in recurrent multiple sclerosis despite its history of market withdrawal due to lethal cases. We have carried out a bibliometric analysis of this drug from 1999 to February 2020 in order to assess the real impact of the use natalizumab with the goal to identify the key articles that sustain the current knowledge on the therapeutic possibilities of this compound. We have extracted from the Web of Science the top 100 most cited records (T100) and tabulated data on the journal, authors, publication year, number of citations, countries and institutions of publication, T100-records, citation density and citations per record of the works. The 100 most cited articles were selected from a total of 32,507 citations out of 2817 publications with an h-number of 74, 11.54 citations/publication, and a density of 1544.79 citations/year. Citations ranged from 63 of the paper placed in the 100th position (T100) to 1940 of the paper in the first position (T1). T2 was cited 888 times, and the difference in the number of citations between T1 and T2 was higher than that between T2 and T10. T1, T2 and T3 are clinical trials. When articles are arranged by institution and nationality having more than 10 T100 articles, biotechnology company Biogen and the USA, respectively, lead the ranking, but we also find that 8 out of 10 are academic European institutions. A co-authorship analysis reveals an intense collaborative activity between countries and institutions. We conclude that the clinical and academic communities have shown a sustained interest in natalizumab for the therapy of recurrent multiple sclerosis over the last 20 years.
MeSH term(s)	Bibliometrics ; Humans ; Immunologic Factors/therapeutic use ; Multiple Sclerosis/drug therapy ; Natalizumab/therapeutic use ; Periodicals as Topic/standards ; Periodicals as Topic/trends
Chemical Substances	Immunologic Factors ; Natalizumab
Language	English
Publishing date	2020-09-08
Publishing country	Netherlands
Document type	Evaluation Study ; Journal Article
ZDB-ID	8335-5
ISSN	1872-8421 ; 0165-5728
ISSN (online)	1872-8421
ISSN	0165-5728
DOI	10.1016/j.jneuroim.2020.577379
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Article ; Online: A Bibliometric Evaluation of the Top 100 Cited Dimethyl Fumarate Articles.

García-Fernández, Francisco Javier / García-Fernández, Alba Estela / Ikuta, Ichiro / Nava, Eduardo / Solis García Del Pozo, Julian / Jordan, Joaquin / Galindo, Maria F

Molecules (Basel, Switzerland)

2021 Volume 26, Issue 4

Abstract: Dimethyl fumarate is a cytoprotective and immunomodulatory drug used in the treatment of multiple sclerosis. We performed a bibliometric study examining the characteristics and trends of the top 100 cited articles that include dimethyl fumarate in the ... ...

Abstract	Dimethyl fumarate is a cytoprotective and immunomodulatory drug used in the treatment of multiple sclerosis. We performed a bibliometric study examining the characteristics and trends of the top 100 cited articles that include dimethyl fumarate in the title. On 21 September 2020 we carried out an electronic search in the Web of Science (WOS), seeking articles that include the following terms within the title: dimethyl fumarate, BG-12, or Tecfidera. To focus our investigation on original research, we refined the search to include only articles, early access, others, case report, and clinical trials. We obtained a total of 1115 items, which were cited 7169 times, had a citation density of 6.43 citations/item, and an h-index of 40. Around 2010, there was a jump in the number of published articles per year, rising from 5 articles/year up to 12 articles/year. We sorted all the items by the number of citations and selected the top 100 most cited (T100). The T100 had 4164 citations, with a density of 37 citations/year and contained 16 classic research articles. They were published between 1961 and 2018; the years 2010-2018 amassed nearly 80% of the T100. We noted 17 research areas with articles in the T100. Of these, the number one ranking went to neurosciences/neurology with 39 articles, and chemistry ranked second on the T100 list with 14 items. We noticed that the percentage of articles belonging to different journals changed depending on the time period. Chemistry held the highest number of papers during 1961-2000, while pharmacology andneurosciences/neurology led the 2001-2018 interval. A total of 478 authors from 145 institutions and 25 countries were included in the T100 ranking. The paper by Gold R et al. was the most successful with 14 articles, 1.823 citations and a density of 140.23 citations/year. The biotechnological company Biogen led the T100 list with 20 articles. With 59 published articles, the USA was the leading country in publications. We concluded that this study analyzed the use of and research on dimethyl fumarate from a different perspective, which will allow the readership (expert or not) to understand the relevance of classic and recent literature on this topic.
MeSH term(s)	Authorship ; Bibliometrics ; Dimethyl Fumarate/chemistry ; Publications
Chemical Substances	Dimethyl Fumarate (FO2303MNI2)
Language	English
Publishing date	2021-02-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules26041085
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Article ; Online: Characterization of mitophagy in the 6-hydoxydopamine Parkinson's disease model.

Solesio, Maria E / Saez-Atienzar, Sara / Jordán, Joaquin / Galindo, Maria F

Toxicological sciences : an official journal of the Society of Toxicology

2012 Volume 129, Issue 2, Page(s) 411–420

Abstract: In the present study, the activation of autophagy and its interaction with the mitochondrial fission machinery was investigated in an experimental model of Parkinson's disease. The addition of 50µM 6-hydroxydopamine (6-OHDA) to the dopaminergic cell line ...

Abstract	In the present study, the activation of autophagy and its interaction with the mitochondrial fission machinery was investigated in an experimental model of Parkinson's disease. The addition of 50µM 6-hydroxydopamine (6-OHDA) to the dopaminergic cell line SH-SY5Y profoundly stimulated formation of autophagosomes within 12h. Under these conditions, mitochondrial fission was also activated in a sustained manner, but this occurred at earlier time points (after 3h). Upon 6-OHDA treatment, dynamin-related protein 1 (Drp1) transiently translocated to mitochondria, with increased levels of mitochondrial Drp1 being observed after 3 and 9h. Pharmacological inhibition of Drp1, through treatment with the mitochondrial-division inhibitor-1 (mdivi-1), resulted in the abrogation of mitochondrial fission and in a decrease of the number of autophagic cells. In addition, 6-OHDA failed to induce the expression of the proapoptotic protein Bax in total cellular extracts although it did induce its migration to mitochondria. In our model, Bax migrated later than Drp1. However, Drp1 inhibition did not block Bax migration. These results show that reactive oxygen species but not quinone derivates act as mediators of autophagy at an early stage of the process. 6-OHDA induces hydrogen peroxide production, which was placed upstream of mitochondrial fission, given that mdivi-1 did not abrogate this increase. Furthermore, the 6-OHDA-induced activation of autophagy was also suppressed by addition of the free radical scavengers TEMPOL and MnTBAP. This effect could be reproduced by the addition of hydrogen peroxide, but not with aged 6-OHDA. To our knowledge, this is the first detailed study highlighting the various mediators that are implicated in mitochondrial alterations and autophagy of cells in response to 6-OHDA.
MeSH term(s)	Animals ; Cell Line ; Disease Models, Animal ; Humans ; Mitochondrial Degradation/drug effects ; Oxidopamine/toxicity ; Parkinson Disease/etiology ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Oxygen Species ; Oxidopamine (8HW4YBZ748)
Language	English
Publishing date	2012-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1420885-4
ISSN	1096-0929 ; 1096-6080
ISSN (online)	1096-0929
ISSN	1096-6080
DOI	10.1093/toxsci/kfs218
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Zs.A 1709: Show issues

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Article ; Online: 3-Nitropropionic acid induces autophagy by forming mitochondrial permeability transition pores rather than activating the mitochondrial fission pathway.

Solesio, Maria E / Saez-Atienzar, Sara / Jordan, Joaquin / Galindo, Maria F

British journal of pharmacology

2012 Volume 168, Issue 1, Page(s) 63–75

Abstract: Background and purpose: Huntington's disease is a neurodegenerative process associated with mitochondrial alterations. Inhibitors of the electron-transport channel complex II, such as 3-nitropropionic acid (3NP), are used to study the molecular and ... ...

Abstract	Background and purpose: Huntington's disease is a neurodegenerative process associated with mitochondrial alterations. Inhibitors of the electron-transport channel complex II, such as 3-nitropropionic acid (3NP), are used to study the molecular and cellular pathways involved in this disease. We studied the effect of 3NP on mitochondrial morphology and its involvement in macrophagy. Experimental approach: Pharmacological and biochemical methods were used to characterize the effects of 3NP on autophagy and mitochondrial morphology. SH-SY5Y cells were transfected with GFP-LC3, GFP-Drp1 or GFP-Bax to ascertain their role and intracellular localization after 3NP treatment using confocal microscopy. Key results: Untreated SH-SY5Y cells presented a long, tubular and filamentous net of mitochondria. After 3NP (5 mM) treatment, mitochondria became shorter and rounder. 3NP induced formation of mitochondrial permeability transition pores, both in cell cultures and in isolated liver mitochondria, and this process was inhibited by cyclosporin A. Participation of the mitochondrial fission pathway was excluded because 3NP did not induce translocation of the dynamin-related protein 1 (Drp1) to the mitochondria. The Drp1 inhibitor Mdivi-1 did not affect the observed changes in mitochondrial morphology. Finally, scavengers of reactive oxygen species failed to prevent mitochondrial alterations, while cyclosporin A, but not Mdivi-1, prevented the generation of ROS. Conclusions and implications: There was a direct correlation between formation of mitochondrial permeability transition pores and autophagy induced by 3NP treatment. Activation of autophagy preceded the apoptotic process and was mediated, at least partly, by formation of reactive oxygen species and mitochondrial permeability transition pores.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Autophagy/drug effects ; Cells, Cultured ; Cyclosporine/pharmacology ; Dynamins ; Electron Transport Complex II/metabolism ; Enzyme Inhibitors/pharmacology ; GTP Phosphohydrolases/drug effects ; GTP Phosphohydrolases/genetics ; Humans ; Male ; Mice ; Microscopy, Confocal ; Microtubule-Associated Proteins/drug effects ; Microtubule-Associated Proteins/genetics ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitochondrial Dynamics ; Mitochondrial Membrane Transport Proteins/analysis ; Mitochondrial Membrane Transport Proteins/antagonists & inhibitors ; Mitochondrial Membrane Transport Proteins/biosynthesis ; Mitochondrial Membrane Transport Proteins/drug effects ; Mitochondrial Membrane Transport Proteins/metabolism ; Mitochondrial Permeability Transition Pore ; Mitochondrial Proteins/drug effects ; Mitochondrial Proteins/genetics ; Nitro Compounds/pharmacology ; Permeability/drug effects ; Propionates/pharmacology ; Rats, Wistar ; Reactive Oxygen Species/metabolism ; Translocation, Genetic/drug effects ; bcl-2-Associated X Protein/genetics ; bcl-2-Associated X Protein/metabolism
Chemical Substances	Enzyme Inhibitors ; Microtubule-Associated Proteins ; Mitochondrial Membrane Transport Proteins ; Mitochondrial Permeability Transition Pore ; Mitochondrial Proteins ; Nitro Compounds ; Propionates ; Reactive Oxygen Species ; bcl-2-Associated X Protein ; Cyclosporine (83HN0GTJ6D) ; Electron Transport Complex II (EC 1.3.5.1) ; GTP Phosphohydrolases (EC 3.6.1.-) ; DNM1L protein, human (EC 3.6.5.5) ; Dynamins (EC 3.6.5.5) ; 3-nitropropionic acid (QY4L0FOX0D)
Language	English
Publishing date	2012-04-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/j.1476-5381.2012.01994.x
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Article ; Online: Mitochondria: the headquarters in ischemia-induced neuronal death.

Jordan, Joaquin / de Groot, Piet W J / Galindo, Maria F

Central nervous system agents in medicinal chemistry

2011 Volume 11, Issue 2, Page(s) 98–106

Abstract: Due to a lack of efficient treatments, searching for novel therapies against acute ischemic stroke represents one of the main fields in neuropharmacology. In this review we summarize and discuss the role of mitochondrial participation in ischemia-induced ...

Abstract	Due to a lack of efficient treatments, searching for novel therapies against acute ischemic stroke represents one of the main fields in neuropharmacology. In this review we summarize and discuss the role of mitochondrial participation in ischemia-induced neuronal death. Mitochondria are regarded as the main link between cellular stress signals and the execution of programmed death of nerve cells. Since it was described that the release of mitochondrial proteins such as cytochrome c, apoptosis inducing factor and endonuclease G are key elements in cell death pathways, they have been the focus of cell death studies. Changes in the permeability of the mitochondrial outer membrane result in a non-reversible step in cell death processes. Cytochrome c released from mitochondria binds in the cytoplasm to Apaf-1 to initiate the formation of an apoptosome, which then binds pro-caspase-9. Active caspase-9 cleaves "executioner" caspases, which in turn proceed to cleave key substrates in the cell. Thus, the identification of new targets might enable establishment of novel strategies for therapeutic research, in this case based on the molecular mechanisms of mitochondrial pathways, to improve the development of compounds for treatment of ischemia.
MeSH term(s)	Anti-Bacterial Agents/pharmacology ; Apoptotic Protease-Activating Factor 1/metabolism ; Brain Ischemia/pathology ; Calcium/metabolism ; Cell Death/physiology ; Cytochromes c/metabolism ; Energy Metabolism/drug effects ; Homeostasis ; Minocycline/pharmacology ; Mitochondria/drug effects ; Mitochondria/physiology ; Mitochondria/ultrastructure ; Mitochondrial Membranes/metabolism ; Neurons/cytology ; Neurons/pathology ; Neurons/physiology ; Permeability ; Reactive Oxygen Species/metabolism
Chemical Substances	Anti-Bacterial Agents ; Apoptotic Protease-Activating Factor 1 ; Reactive Oxygen Species ; Cytochromes c (9007-43-6) ; Minocycline (FYY3R43WGO) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2011-04-22
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2227560-5
ISSN	1875-6166 ; 1871-5249
ISSN (online)	1875-6166
ISSN	1871-5249
DOI	10.2174/187152411796011358
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Zs.A 5594: Show issues

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Article ; Online: The senescence-accelerated mouse prone-8 (SAM-P8) oxidative stress is associated with upregulation of renal NADPH oxidase system.

Baltanás, Ana / Solesio, Maria E / Zalba, Guillermo / Galindo, María F / Fortuño, Ana / Jordán, Joaquín

Journal of physiology and biochemistry

2013 Volume 69, Issue 4, Page(s) 927–935

Abstract: Herein, we investigate whether the NADPH oxidase might be playing a key role in the degree of oxidative stress in the senescence-accelerated mouse prone-8 (SAM-P8). To this end, the activity and expression of the NADPH oxidase, the ratio of glutathione ... ...

Abstract	Herein, we investigate whether the NADPH oxidase might be playing a key role in the degree of oxidative stress in the senescence-accelerated mouse prone-8 (SAM-P8). To this end, the activity and expression of the NADPH oxidase, the ratio of glutathione and glutathione disulfides (GSH/GSSG), and the levels of malonyl dialdehyde (MDA) and nitrotyrosine (NT) were determined in renal tissue from SAM-P8 mice at the age of 1 and 6 months. The senescence-accelerated-resistant mouse (SAM-R1) was used as control. At the age of 1 month, NADPH oxidase activity and Nox2 protein expression were higher in SAM-P8 than in SAM-R1 mice. However, we found no differences in the GSH/GSSG ratio, MDA, NT, and Nox4 levels between both groups of animals. At the age of 6 months, SAM-R1 mice in comparison to SAM-P8 mice showed an increase in NADPH oxidase activity, which is associated with higher levels of NT and increased Nox4 and Nox2 expression levels. Furthermore, we found oxidative stress hallmarks including depletion in GSH/GSSG ratio and increase in MDA levels in the kidney of SAM-P8 mice. Finally, NADPH oxidase activity positively correlated with Nox2 expression in all the animals (r = 0.382, P < 0.05). Taken together, our data allow us to suggest that an increase in NADPH oxidase activity might be an early hallmark to predict future oxidative stress in renal tissue during the aging process that takes place in SAM-P8 mice.
MeSH term(s)	Aging/genetics ; Aging/metabolism ; Animals ; Gene Expression ; Glutathione/metabolism ; Glutathione Disulfide/metabolism ; Kidney/metabolism ; Lipid Peroxidation ; Male ; Malondialdehyde/metabolism ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Transgenic ; NADPH Oxidase 2 ; NADPH Oxidase 4 ; NADPH Oxidases/genetics ; NADPH Oxidases/metabolism ; Oxidation-Reduction ; Oxidative Stress ; Tyrosine/analogs & derivatives ; Tyrosine/metabolism ; Up-Regulation
Chemical Substances	Membrane Glycoproteins ; 3-nitrotyrosine (3604-79-3) ; Tyrosine (42HK56048U) ; Malondialdehyde (4Y8F71G49Q) ; Cybb protein, mouse (EC 1.6.3.-) ; NADPH Oxidase 2 (EC 1.6.3.-) ; NADPH Oxidase 4 (EC 1.6.3.-) ; NADPH Oxidases (EC 1.6.3.-) ; Nox4 protein, mouse (EC 1.6.3.-) ; Glutathione (GAN16C9B8O) ; Glutathione Disulfide (ULW86O013H)
Language	English
Publishing date	2013-07-11
Publishing country	Spain
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1325104-1
ISSN	1877-8755 ; 0034-9402 ; 1138-7548
ISSN (online)	1877-8755
ISSN	0034-9402 ; 1138-7548
DOI	10.1007/s13105-013-0271-6
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Article ; Online: Mitochondrial dynamics and mitophagy in the 6-hydroxydopamine preclinical model of Parkinson's disease.

Galindo, Maria F / Solesio, Maria E / Atienzar-Aroca, Sandra / Zamora, Maria J / Jordán Bueso, Joaquín

Parkinson's disease

2012 Volume 2012, Page(s) 131058

Abstract: We discuss the participation of mitochondrial dynamics and autophagy in the 6-hydroxidopamine-induced Parkinson's disease model. The regulation of dynamic mitochondrial processes such as fusion, fission, and mitophagy has been shown to be an important ... ...

Abstract	We discuss the participation of mitochondrial dynamics and autophagy in the 6-hydroxidopamine-induced Parkinson's disease model. The regulation of dynamic mitochondrial processes such as fusion, fission, and mitophagy has been shown to be an important mechanism controlling cellular fate. An imbalance in mitochondrial dynamics may contribute to both familial and sporadic neurodegenerative diseases including Parkinson's disease. With special attention we address the role of second messengers as the role of reactive oxygen species and the mitochondria as the headquarters of cell death. The role of molecular signaling pathways, for instance, the participation of Dynamin-related protein 1(Drp1), will also be addressed. Furthermore evidence demonstrates the therapeutic potential of small-molecule inhibitors of mitochondrial division in Parkinson's disease. For instance, pharmacological inhibition of Drp1, through treatment with the mitochondrial division inhibitor-1, results in the abrogation of mitochondrial fission and in a decrease of the number of autophagic cells. Deciphering the signaling cascades that underlie mitophagy triggered by 6-OHDA, as well as the mechanisms that determine the selectivity of this response, will help to better understand this process and may have impact on human treatment strategies of Parkinson's disease.
Language	English
Publishing date	2012-08-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2573854-9
ISSN	2042-0080 ; 2090-8083
ISSN (online)	2042-0080
ISSN	2090-8083
DOI	10.1155/2012/131058
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Article: Mitochondrial biology in Alzheimer's disease pathogenesis

Galindo, María F / Ikuta, Ichiro / Zhu, Xiongwei / Casadesus, Gemma / Jordán, Joaquín

Journal of neurochemistry. 2010 Aug., v. 114, no. 4

2010

Abstract: J. Neurochem. (2010) 114, 933-945. Despite the increasing knowledge of Alzheimer's disease (AD) management with novel pharmacologic agents, most of them are only transiently fixing symptomatic pathology. Currently there is rapid growth in the field of ... ...

Abstract	J. Neurochem. (2010) 114, 933-945. Despite the increasing knowledge of Alzheimer's disease (AD) management with novel pharmacologic agents, most of them are only transiently fixing symptomatic pathology. Currently there is rapid growth in the field of neuroprotective pharmacology and increasing focus on the involvement of mitochondria in this devastating disease. This review is directed at understanding the role of mitochondria-mediated pathways in AD and integrating basic biology of the mitochondria with knowledge of possible pharmacologic targets for AD treatment in an attempt to elucidate novel mitochondria-driven therapeutic interventions useful to both clinical and basic research.
Keywords	apoptosis ; reactive oxygen species
Language	English
Dates of publication	2010-08
Size	p. 933-945.
Publisher	Blackwell Publishing Ltd
Publishing place	Oxford, UK
Document type	Article
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/j.1471-4159.2010.06814.x
Database	NAL-Catalogue (AGRICOLA)

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