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Article ; Online: Corrigendum to "Slower Dynamics and Aged Mitochondria in Sporadic Alzheimer's Disease".

Martín-Maestro, Patricia / Gargini, Ricardo / García, Esther / Perry, George / Avila, Jesús / García-Escudero, Vega

Oxidative medicine and cellular longevity

2021 Volume 2021, Page(s) 1643631

Abstract: This corrects the article DOI: 10.1155/2017/9302761.]. ...

Abstract	[This corrects the article DOI: 10.1155/2017/9302761.].
Language	English
Publishing date	2021-01-14
Publishing country	United States
Document type	Published Erratum
ISSN	1942-0994
ISSN (online)	1942-0994
DOI	10.1155/2021/1643631
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Article ; Online: Mitophagy Failure in APP and Tau Overexpression Model of Alzheimer's Disease.

Martín-Maestro, Patricia / Gargini, Ricardo / García, Esther / Simón, Diana / Avila, Jesús / García-Escudero, Vega

Journal of Alzheimer's disease : JAD

2019 Volume 70, Issue 2, Page(s) 525–540

Abstract: Mitochondrial alterations and oxidative stress are common features of Alzheimer's disease brain and peripheral tissues. Moreover, mitochondrial recycling process by autophagy has been found altered in the sporadic form of the disease. However, the ... ...

Abstract	Mitochondrial alterations and oxidative stress are common features of Alzheimer's disease brain and peripheral tissues. Moreover, mitochondrial recycling process by autophagy has been found altered in the sporadic form of the disease. However, the contribution of the main proteins involved in this pathology such as amyloid-β protein precursor (AβPP) and tau needs to be achieved. With this aim, human unmodified fibroblasts were transduced with lentivectors encoding APP and Tau and treated with CCCP to study the mitophagy process. Both AβPP and tau separately increased autophagy flux mainly by improving degradation phase. However, in the specific case of mitophagy, labeling of mitochondria by PINK1 and PARK2 to be degraded by autophagy seemed reduced, which correlates with the long-term accumulation of mitochondria. Nevertheless, the combination of tau and AβPP was necessary to cause a mitophagy functional impairment reflected in the accumulation of depolarized mitochondria labeled by PINK1. The overexpression of Tau and APP recapitulates the mitophagy failure previously found in sporadic Alzheimer's disease.
MeSH term(s)	Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Protein Precursor/biosynthesis ; Amyloid beta-Protein Precursor/genetics ; Cells, Cultured ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Gene Expression ; Humans ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitophagy/physiology ; tau Proteins/biosynthesis ; tau Proteins/genetics
Chemical Substances	Amyloid beta-Protein Precursor ; MAPT protein, human ; tau Proteins
Language	English
Publishing date	2019-06-28
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-190086
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Article ; Online: Suicidal behaviour recurrence in psychiatric emergency departments of patients without a prior suicide attempt, index and reattempters: A prospective study.

López-Goñi, José Javier / Goñi-Sarriés, Adriana / Azcárate-Jiménez, Leire / Sabater-Maestro, Pablo

Revista de psiquiatria y salud mental

2018 Volume 13, Issue 4, Page(s) 192–201

Abstract: Introduction: There has been little change in the incidence of suicidal behaviour and reattempts in recent years. Evidence is needed on the incidence of suicidal behaviour in the psychiatric population and its follow-up.: Material and method: A ... ...

Title translation	Repetición de conductas suicidas en urgencias psiquiátricas en pacientes sin intentos previos, index y repetidores: un estudio prospectivo.
Abstract	Introduction: There has been little change in the incidence of suicidal behaviour and reattempts in recent years. Evidence is needed on the incidence of suicidal behaviour in the psychiatric population and its follow-up. Material and method: A prospective multi-centre case-control study. The sample covered the cases of 440 patients seen as psychiatric emergencies. For this purpose, we used the Vital Adverse Event Scale by Brugha and screening with the Columbia Scale. The sample was divided into three groups: patients without prior suicide attempts, patients with an index attempt and patients with more than one attempt. At two years, the clinical histories of these patients were reviewed, assessing for suicidal behaviour. Results: A total of 49.1% (n=216) of the patients required urgent psychiatric care during the follow-up period, and 2.7% eventually committed suicide. The data shows a differential profile between the three groups analysed. Among them, the group of reattempters required the highest number of interventions regarding suicide behaviour (11.0%; χ Conclusions: The results show the need for assessing suicidal behaviour for all patients who receive psychiatric urgent care, including during the follow-up period. A more thorough control should be performed during the first months for patients without prior suicide attempts, and longer periods for those patients who have already tried to commit suicide.
Language	Spanish
Publishing date	2018-11-23
Publishing country	Spain
Document type	Journal Article
ISSN	2173-5050
ISSN (online)	2173-5050
DOI	10.1016/j.rpsm.2018.07.003
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Article ; Online: Autophagy Induction by Bexarotene Promotes Mitophagy in Presenilin 1 Familial Alzheimer's Disease iPSC-Derived Neural Stem Cells.

Martín-Maestro, Patricia / Sproul, Andrew / Martinez, Hector / Paquet, Dominik / Gerges, Meri / Noggle, Scott / Starkov, Anatoly A

Molecular neurobiology

2019 Volume 56, Issue 12, Page(s) 8220–8236

Abstract: Adult neurogenesis defects have been demonstrated in the brains of Alzheimer's disease (AD) patients. The neurogenesis impairment is an early critical event in the course of familiar AD (FAD) associated with neuronal loss. It was suggested that ... ...

Abstract	Adult neurogenesis defects have been demonstrated in the brains of Alzheimer's disease (AD) patients. The neurogenesis impairment is an early critical event in the course of familiar AD (FAD) associated with neuronal loss. It was suggested that neurologic dysfunction in AD may be caused by impaired functioning of hippocampal neural stem cells (NSCs). Multiple metabolic and structural abnormalities in neural mitochondria have long been suspected to play a critical role in AD pathophysiology. We hypothesize that the cause of such abnormalities could be defective elimination of damaged mitochondria. In the present study, we evaluated mitophagy efficacy in a cellular AD model, hiPSC-derived NSCs harboring the FAD-associated PS1 M146L mutation. We found several mitochondrial respiratory chain defects such as lower expression levels of cytochrome c oxidase (complex IV), cytochrome c reductase (complex III), succinate dehydrogenase (complex II), NADH:CoQ reductase (complex I), and also ATP synthase (complex V), most of which had been previously associated with AD. The mitochondrial network morphology and abundance in these cells was aberrant. This was associated with a marked mitophagy failure stemming from autophagy induction blockage, and deregulation of the expression of proteins involved in mitochondrial dynamics. We show that treating these cells with autophagy-stimulating drug bexarotene restored autophagy and compensated mitochondrial anomalies in PS1 M146L NSCs, by enhancing the clearance of mitochondria. Our data support the hypothesis that pharmacologically induced mitophagy enhancement is a relevant and novel therapeutic strategy for the treatment of AD.
MeSH term(s)	Alzheimer Disease/pathology ; Autophagy/drug effects ; Bexarotene/pharmacology ; DNA, Mitochondrial/genetics ; Humans ; Induced Pluripotent Stem Cells/drug effects ; Induced Pluripotent Stem Cells/metabolism ; Induced Pluripotent Stem Cells/pathology ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitophagy/drug effects ; Neural Stem Cells/drug effects ; Neural Stem Cells/metabolism ; Neural Stem Cells/pathology ; Presenilin-1/genetics
Chemical Substances	DNA, Mitochondrial ; Presenilin-1 ; Bexarotene (A61RXM4375)
Language	English
Publishing date	2019-06-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-019-01665-y
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Article ; Online: Slower Dynamics and Aged Mitochondria in Sporadic Alzheimer's Disease.

Martín-Maestro, Patricia / Gargini, Ricardo / García, Esther / Perry, George / Avila, Jesús / García-Escudero, Vega

Oxidative medicine and cellular longevity

2017 Volume 2017, Page(s) 9302761

Abstract: Sporadic Alzheimer's disease corresponds to 95% of cases whose origin is multifactorial and elusive. Mitochondrial dysfunction is a major feature of Alzheimer's pathology, which might be one of the early events that trigger downstream principal events. ... ...

Abstract	Sporadic Alzheimer's disease corresponds to 95% of cases whose origin is multifactorial and elusive. Mitochondrial dysfunction is a major feature of Alzheimer's pathology, which might be one of the early events that trigger downstream principal events. Here, we show that multiple genes that control mitochondrial homeostasis, including fission and fusion, are downregulated in Alzheimer's patients. Additionally, we demonstrate that some of these dysregulations, such as diminished DLP1 levels and its mitochondrial localization, as well as reduced STOML2 and MFN2 fusion protein levels, take place in fibroblasts from sporadic Alzheimer's disease patients. The analysis of mitochondrial network disruption using CCCP indicates that the patients' fibroblasts exhibit slower dynamics and mitochondrial membrane potential recovery. These defects lead to strong accumulation of aged mitochondria in Alzheimer's fibroblasts. Accordingly, the analysis of autophagy and mitophagy involved genes in the patients demonstrates a downregulation indicating that the recycling mechanism of these aged mitochondria might be impaired. Our data reinforce the idea that mitochondrial dysfunction is one of the key early events of the disease intimately related with aging.
MeSH term(s)	Aged ; Aging ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Autophagy/drug effects ; Blood Proteins/metabolism ; Brain/metabolism ; Cells, Cultured ; Doxorubicin/toxicity ; Dynamins ; Female ; Fibroblasts/cytology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; GTP Phosphohydrolases/metabolism ; Humans ; Male ; Membrane Potential, Mitochondrial/drug effects ; Membrane Proteins/metabolism ; Microscopy, Fluorescence ; Microtubule-Associated Proteins/metabolism ; Middle Aged ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondrial Dynamics ; Mitochondrial Proteins/metabolism ; Mitophagy/drug effects ; Oligonucleotide Array Sequence Analysis
Chemical Substances	Blood Proteins ; Membrane Proteins ; Microtubule-Associated Proteins ; Mitochondrial Proteins ; STOML2 protein, human ; Doxorubicin (80168379AG) ; GTP Phosphohydrolases (EC 3.6.1.-) ; MFN2 protein, human (EC 3.6.1.-) ; DNM1L protein, human (EC 3.6.5.5) ; Dynamins (EC 3.6.5.5)
Language	English
Publishing date	2017-10-19
Publishing country	United States
Document type	Journal Article
ISSN	1942-0994
ISSN (online)	1942-0994
DOI	10.1155/2017/9302761
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Article ; Online: PARK2 enhancement is able to compensate mitophagy alterations found in sporadic Alzheimer's disease.

Martín-Maestro, Patricia / Gargini, Ricardo / Perry, George / Avila, Jesús / García-Escudero, Vega

Human molecular genetics

2016 Volume 25, Issue 4, Page(s) 792–806

Abstract: Mitochondrial anomalies have been previously reported in patients' brain and peripheral tissue, suggesting their relevance in sporadic Alzheimer's disease (AD). The present work evaluates mitochondrial function and recycling in human fibroblasts and ... ...

Abstract	Mitochondrial anomalies have been previously reported in patients' brain and peripheral tissue, suggesting their relevance in sporadic Alzheimer's disease (AD). The present work evaluates mitochondrial function and recycling in human fibroblasts and brain biopsies. Functional studies using patients' skin fibroblasts showed slower mitochondrial membrane potential recovery after a mitochondrial insult together with alterations in lysosomes and autophagy, accompanied by an increase of oxidized and ubiquitinated proteins. Impairment in mitophagy has been proven in these cells due to diminished PARK2 and insufficient vesicle induction, accumulating depolarized mitochondria and PINK1. Augmented Δ1 PINK1 fragment levels suggest an inhibitory effect over PARK2 translocation to the mitochondria, causing the accumulation of activated PINK1. Moreover, the overexpression of PARK2 diminished ubiquitinated proteins accumulation, improves its targeting to mitochondria and potentiates autophagic vesicle synthesis. This allows the reversion of mitophagy failure reflected in the recovery of membrane potential and the decrease of PINK1 and mitochondria accumulation. Sporadic AD fibroblasts exhibited alterations similar to what it could be found in patients' hippocampal samples at early stages of the disease, where there was an accumulation of PINK1 and Δ1 PINK1 together with abnormally increased mitochondrial content. Our findings indicate that mitophagy alterations can be considered a new hallmark of sporadic AD and validate the use of fibroblasts for modelling this pathology.
MeSH term(s)	Aged ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Alzheimer Disease/therapy ; Autophagy/physiology ; Brain/metabolism ; Brain/pathology ; Case-Control Studies ; Female ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Humans ; Lysosomes/metabolism ; Lysosomes/pathology ; Male ; Membrane Potential, Mitochondrial/physiology ; Middle Aged ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitochondrial Degradation/physiology ; Mitochondrial Proteins/metabolism ; Primary Cell Culture ; Protein Kinases/metabolism ; Transfection ; Ubiquitin-Protein Ligases/administration & dosage ; Ubiquitin-Protein Ligases/biosynthesis ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	Mitochondrial Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; parkin protein (EC 2.3.2.27) ; Protein Kinases (EC 2.7.-) ; PTEN-induced putative kinase (EC 2.7.11.1)
Language	English
Publishing date	2016-02-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/ddv616
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Zs.A 3469: Show issues

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Article ; Online: Deconstructing mitochondrial dysfunction in Alzheimer disease.

García-Escudero, Vega / Martín-Maestro, Patricia / Perry, George / Avila, Jesús

Oxidative medicine and cellular longevity

2013 Volume 2013, Page(s) 162152

Abstract: There is mounting evidence showing that mitochondrial damage plays an important role in Alzheimer disease. Increased oxygen species generation and deficient mitochondrial dynamic balance have been suggested to be the reason as well as the consequence of ... ...

Abstract	There is mounting evidence showing that mitochondrial damage plays an important role in Alzheimer disease. Increased oxygen species generation and deficient mitochondrial dynamic balance have been suggested to be the reason as well as the consequence of Alzheimer-related pathology. Mitochondrial damage has been related to amyloid-beta or tau pathology or to the presence of specific presenilin-1 mutations. The contribution of these factors to mitochondrial dysfunction is reviewed in this paper. Due to the relevance of mitochondrial alterations in Alzheimer disease, recent works have suggested the therapeutic potential of mitochondrial-targeted antioxidant. On the other hand, autophagy has been demonstrated to play a fundamental role in Alzheimer-related protein stress, and increasing data shows that this pathway is altered in the disease. Moreover, mitochondrial alterations have been related to an insufficient clearance of dysfunctional mitochondria by autophagy. Consequently, different approaches for the removal of damaged mitochondria or to decrease the related oxidative stress in Alzheimer disease have been described. To understand the role of mitochondrial function in Alzheimer disease it is necessary to generate human cellular models which involve living neurons. We have summarized the novel protocols for the generation of neurons by reprogramming or direct transdifferentiation, which offer useful tools to achieve this result.
MeSH term(s)	Alzheimer Disease/drug therapy ; Alzheimer Disease/pathology ; Animals ; Antioxidants/therapeutic use ; Disease Models, Animal ; Humans ; Mitochondria/pathology
Chemical Substances	Antioxidants
Language	English
Publishing date	2013-06-11
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2455981-7
ISSN	1942-0994 ; 1942-0994
ISSN (online)	1942-0994
ISSN	1942-0994
DOI	10.1155/2013/162152
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Article ; Online: Glycogen synthase kinase-3β regulates fractalkine production by altering its trafficking from Golgi to plasma membrane: implications for Alzheimer's disease.

Fuster-Matanzo, Almudena / Jurado-Arjona, Jerónimo / Benvegnù, Stefano / García, Esther / Martín-Maestro, Patricia / Gómez-Sintes, Raquel / Hernández, Félix / Ávila, Jesús

Cellular and molecular life sciences : CMLS

2017 Volume 74, Issue 6, Page(s) 1153–1163

Abstract: Glycogen synthase kinase-3β (GSK-3β) is a serine-threonine kinase implicated in multiple processes and signaling pathways. Its dysregulation is associated with different pathological conditions including Alzheimer's disease (AD). Here we demonstrate how ... ...

Abstract	Glycogen synthase kinase-3β (GSK-3β) is a serine-threonine kinase implicated in multiple processes and signaling pathways. Its dysregulation is associated with different pathological conditions including Alzheimer's disease (AD). Here we demonstrate how changes in GSK-3β activity and/or levels regulate the production and subsequent secretion of fractalkine, a chemokine involved in the immune response that has been linked to AD and to other different neurological disorders. Treatment of primary cultured neurons with GSK-3β inhibitors such as lithium and AR-A014418 decreased full-length fractalkine in total cell extracts. Opposite effects were observed after neuron transduction with a lentiviral vector overexpressing the kinase. Biotinylation assays showed that those changes mainly affect the plasma membrane-associated form of the protein, an observation that positively correlates with changes in the levels of its soluble form. These effects were confirmed in lithium-treated wild type (wt) mice and in GSK-3β transgenic animals, as well as in brain samples from AD patients, evident as age-dependent (animals) or Braak stage dependent changes (humans) in both the membrane-bound and the soluble forms of the protein. Further immunohistochemical analyses demonstrated how GSK-3β exerts these effects by affecting the trafficking of the chemokine from the Golgi to the plasma membrane, in different and opposite ways when the levels/activity of the kinase are increased or decreased. This work provides for the first time a mechanism linking GSK-3β and fractalkine both in vitro and in vivo, with important implications for neurological disorders and especially for AD, in which levels of this chemokine might be useful as a diagnostic tool.
MeSH term(s)	Alzheimer Disease/metabolism ; Animals ; Cell Membrane/metabolism ; Chemokine CX3CL1/metabolism ; Glycogen Synthase Kinase 3 beta/metabolism ; Golgi Apparatus/metabolism ; Humans ; Mice, Inbred C57BL ; Protein Binding ; Protein Transport ; Solubility ; Transport Vesicles/metabolism ; rab GTP-Binding Proteins/metabolism
Chemical Substances	Chemokine CX3CL1 ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; rab GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2017
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-016-2408-6
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Article ; Online: Tau mRNA 3'UTR-to-CDS ratio is increased in Alzheimer disease.

García-Escudero, Vega / Gargini, Ricardo / Martín-Maestro, Patricia / García, Esther / García-Escudero, Ramón / Avila, Jesús

Neuroscience letters

2017 Volume 655, Page(s) 101–108

Abstract: Neurons frequently show an imbalance in expression of the 3' untranslated region (3'UTR) relative to the coding DNA sequence (CDS) region of mature messenger RNAs (mRNA). The ratio varies among different cells or parts of the brain. The Map2 protein ... ...

Abstract	Neurons frequently show an imbalance in expression of the 3' untranslated region (3'UTR) relative to the coding DNA sequence (CDS) region of mature messenger RNAs (mRNA). The ratio varies among different cells or parts of the brain. The Map2 protein levels per cell depend on the 3'UTR-to-CDS ratio rather than the total mRNA amount, which suggests powerful regulation of protein expression by 3'UTR sequences. Here we found that MAPT (the microtubule-associated protein tau gene) 3'UTR levels are particularly high with respect to other genes; indeed, the 3'UTR-to-CDS ratio of MAPT is balanced in healthy brain in mouse and human. The tau protein accumulates in Alzheimer diseased brain. We nonetheless observed that the levels of RNA encoding MAPT/tau were diminished in these patients' brains. To explain this apparently contradictory result, we studied MAPT mRNA stoichiometry in coding and non-coding regions, and found that the 3'UTR-to-CDS ratio was higher in the hippocampus of Alzheimer disease patients, with higher tau protein but lower total mRNA levels. Our data indicate that changes in the 3'UTR-to-CDS ratio have a regulatory role in the disease. Future research should thus consider not only mRNA levels, but also the ratios between coding and non-coding regions.
Language	English
Publishing date	2017-08-10
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2017.07.007
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Article ; Online: Charge-Sign Dependent Cosmic-Ray Modulation Observed with the Calorimetric Electron Telescope on the International Space Station.

Adriani, O / Akaike, Y / Asano, K / Asaoka, Y / Berti, E / Bigongiari, G / Binns, W R / Bongi, M / Brogi, P / Bruno, A / Buckley, J H / Cannady, N / Castellini, G / Checchia, C / Cherry, M L / Collazuol, G / de Nolfo, G A / Ebisawa, K / Ficklin, A W /

Fuke, H / Gonzi, S / Guzik, T G / Hams, T / Hibino, K / Ichimura, M / Ioka, K / Ishizaki, W / Israel, M H / Kasahara, K / Kataoka, J / Kataoka, R / Katayose, Y / Kato, C / Kawanaka, N / Kawakubo, Y / Kobayashi, K / Kohri, K / Krawczynski, H S / Krizmanic, J F / Maestro, P / Marrocchesi, P S / Messineo, A M / Mitchell, J W / Miyake, S / Moiseev, A A / Mori, M / Mori, N / Motz, H M / Munakata, K / Nakahira, S / Nishimura, J / Okuno, S / Ormes, J F / Ozawa, S / Pacini, L / Papini, P / Rauch, B F / Ricciarini, S B / Sakai, K / Sakamoto, T / Sasaki, M / Shimizu, Y / Shiomi, A / Spillantini, P / Stolzi, F / Sugita, S / Sulaj, A / Takita, M / Tamura, T / Terasawa, T / Torii, S / Tsunesada, Y / Uchihori, Y / Vannuccini, E / Wefel, J P / Yamaoka, K / Yanagita, S / Yoshida, A / Yoshida, K / Zober, W V

Physical review letters

2023 Volume 130, Issue 21, Page(s) 211001

Abstract: We present the observation of a charge-sign dependent solar modulation of galactic cosmic rays (GCRs) with the Calorimetric Electron Telescope onboard the International Space Station over 6 yr, corresponding to the positive polarity of the solar magnetic ...

Abstract	We present the observation of a charge-sign dependent solar modulation of galactic cosmic rays (GCRs) with the Calorimetric Electron Telescope onboard the International Space Station over 6 yr, corresponding to the positive polarity of the solar magnetic field. The observed variation of proton count rate is consistent with the neutron monitor count rate, validating our methods for determining the proton count rate. It is observed by the Calorimetric Electron Telescope that both GCR electron and proton count rates at the same average rigidity vary in anticorrelation with the tilt angle of the heliospheric current sheet, while the amplitude of the variation is significantly larger in the electron count rate than in the proton count rate. We show that this observed charge-sign dependence is reproduced by a numerical "drift model" of the GCR transport in the heliosphere. This is a clear signature of the drift effect on the long-term solar modulation observed with a single detector.
MeSH term(s)	Space Flight ; Protons ; Electrons ; Telescopes ; Cosmic Radiation
Chemical Substances	Protons
Language	English
Publishing date	2023-06-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	208853-8
ISSN	1079-7114 ; 0031-9007
ISSN (online)	1079-7114
ISSN	0031-9007
DOI	10.1103/PhysRevLett.130.211001
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