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Article: Impact of Physical Exercise on Melanoma Hallmarks: Current Status of Preclinical and Clinical Research.

Ceci, Claudia / García-Chico, Celia / Atzori, Maria Grazia / Lacal, Pedro Miguel / Lista, Simone / Santos-Lozano, Alejandro / Graziani, Grazia / Pinto-Fraga, José

Journal of Cancer

2024 Volume 15, Issue 1, Page(s) 1–19

Abstract: In recent years, accumulating evidence from preclinical and clinical studies consistently indicated that physical activity/exercise plays a crucial role in reducing the incidence and recurrence of various malignancies, by exerting a beneficial modulation ...

Abstract	In recent years, accumulating evidence from preclinical and clinical studies consistently indicated that physical activity/exercise plays a crucial role in reducing the incidence and recurrence of various malignancies, by exerting a beneficial modulation of cancer hallmarks. Moreover, physical activity is suggested to attenuate certain adverse effects of anticancer therapy, including the reduction of cardiovascular toxicity and symptoms related to depression and anxiety, among others, while preserving muscular strength. In the case of melanoma, the relationship with physical activity has been critically debated. Historically, several cohort studies and meta-analyses reported a positive association between physical activity/exercise and melanoma risk. This association was primarily attributed to outdoor activities that may expose the skin to UV radiation, a well-known risk factor for melanocyte transformation. However, more recent evidence does not support such association and recognizes physical activity/exercise role in both melanoma prevention and progression. Nevertheless, sun protection is recommended during outdoor training to minimize UV radiation exposure. This narrative review summarizes preclinical and clinical data about physical activity effects on melanoma hallmarks. Specifically, experimental evidence is reported concerning (
Language	English
Publishing date	2024-01-01
Publishing country	Australia
Document type	Journal Article ; Review
ZDB-ID	2573318-7
ISSN	1837-9664
ISSN	1837-9664
DOI	10.7150/jca.88559
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Article: Pumping up the Fight against Multiple Sclerosis: The Effects of High-Intensity Resistance Training on Functional Capacity, Muscle Mass, and Axonal Damage.

Maroto-Izquierdo, Sergio / Mulero, Patricia / Menéndez, Héctor / Pinto-Fraga, José / Lista, Simone / Santos-Lozano, Alejandro / Téllez, Nieves

Healthcare (Basel, Switzerland)

2024 Volume 12, Issue 8

Abstract: Background: Resistance training (RT) has been recognized as a beneficial non-pharmacological intervention for multiple sclerosis (MS) patients, but its impact on neurodegeneration is not fully understood. This study aimed to investigate the effects of ... ...

Abstract	Background: Resistance training (RT) has been recognized as a beneficial non-pharmacological intervention for multiple sclerosis (MS) patients, but its impact on neurodegeneration is not fully understood. This study aimed to investigate the effects of high-intensity RT on muscle mass, strength, functional capacity, and axonal damage in MS patients. Methods: Eleven relapsing-remitting MS patients volunteered in this within-subject counterbalanced intervention study. Serum neurofilament light-chain (NfL) concentration, vastus lateralis thickness (VL), timed up-and-go test (TUG), sit-to-stand test (60STS), and maximal voluntary isometric contraction (MVIC) were measured before and after intervention. Participants performed 18 sessions of high-intensity RT (70-80% 1-RM) over 6 weeks. Results: Significant ( Conclusions: A 6-week RT program significantly increased muscle mass, functional capacity, and neuromuscular function while also decreasing serum NfL in MS patients. These results suggest the effectiveness of RT as a non-pharmacological approach to mitigate neurodegeneration while improving functional capacity in MS patients.
Language	English
Publishing date	2024-04-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2721009-1
ISSN	2227-9032
ISSN	2227-9032
DOI	10.3390/healthcare12080837
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Article: Healthcare Professionals' Knowledge about Pediatric Chronic Pain: A Systematic Review.

Pico, Mónica / Matey-Rodríguez, Carmen / Domínguez-García, Ana / Menéndez, Héctor / Lista, Simone / Santos-Lozano, Alejandro

Children (Basel, Switzerland)

2023 Volume 10, Issue 4

Abstract: Pediatric chronic pain is a common public health problem with a high prevalence among children and adolescents. The aim of this study was to review the current knowledge of health professionals on pediatric chronic pain between 15-30% among children and ... ...

Abstract	Pediatric chronic pain is a common public health problem with a high prevalence among children and adolescents. The aim of this study was to review the current knowledge of health professionals on pediatric chronic pain between 15-30% among children and adolescents. However, since this is an underdiagnosed condition, it is inadequately treated by health professionals. To this aim, a systematic review was carried out based on a search of the electronic literature databases (PubMed and Web of Science), resulting in 14 articles that met the inclusion criteria. The analysis of these articles seems to show a certain degree of heterogeneity in the surveyed professionals about the awareness of this concept, especially regarding its etiology, assessment, and management. In addition, the extent of knowledge of the health professionals seems to be insufficient regarding these aspects of pediatric chronic pain. Hence, the knowledge of the health professionals is unrelated to recent research that identifies central hyperexcitability as the primary factor affecting the onset, persistence, and management of pediatric chronic pain.
Language	English
Publishing date	2023-03-31
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2732685-8
ISSN	2227-9067
ISSN	2227-9067
DOI	10.3390/children10040665
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Article ; Online: A critical appraisal of blood-based biomarkers for Alzheimer's disease.

Lista, Simone / Mapstone, Mark / Caraci, Filippo / Emanuele, Enzo / López-Ortiz, Susana / Martín-Hernández, Juan / Triaca, Viviana / Imbimbo, Camillo / Gabelle, Audrey / Mielke, Michelle M / Nisticò, Robert / Santos-Lozano, Alejandro / Imbimbo, Bruno P

Ageing research reviews

2024 Volume 96, Page(s) 102290

Abstract: Biomarkers that predict the clinical onset of Alzheimer's disease (AD) enable the identification of individuals in the early, preclinical stages of the disease. Detecting AD at this point may allow for more effective therapeutic interventions and ... ...

Abstract	Biomarkers that predict the clinical onset of Alzheimer's disease (AD) enable the identification of individuals in the early, preclinical stages of the disease. Detecting AD at this point may allow for more effective therapeutic interventions and optimized enrollment for clinical trials of novel drugs. The current biological diagnosis of AD is based on the AT(N) classification system with the measurement of brain deposition of amyloid-β (Aβ) ("A"), tau pathology ("T"), and neurodegeneration ("N"). Diagnostic cut-offs for Aβ
MeSH term(s)	Humans ; Alzheimer Disease/metabolism ; tau Proteins ; Cross-Sectional Studies ; Amyloid beta-Peptides ; Biomarkers/cerebrospinal fluid
Chemical Substances	tau Proteins ; Amyloid beta-Peptides ; Biomarkers
Language	English
Publishing date	2024-04-04
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2075672-0
ISSN	1872-9649 ; 1568-1637
ISSN (online)	1872-9649
ISSN	1568-1637
DOI	10.1016/j.arr.2024.102290
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Article ; Online: Monitoring synaptic pathology in Alzheimer's disease through fluid and PET imaging biomarkers: a comprehensive review and future perspectives.

Lista, Simone / Santos-Lozano, Alejandro / Emanuele, Enzo / Mercuri, Nicola B / Gabelle, Audrey / López-Ortiz, Susana / Martín-Hernández, Juan / Maisto, Nunzia / Imbimbo, Camillo / Caraci, Filippo / Imbimbo, Bruno P / Zetterberg, Henrik / Nisticò, Robert

Molecular psychiatry

2024

Abstract: Alzheimer's disease (AD) is currently constrained by limited clinical treatment options. The initial pathophysiological event, which can be traced back to decades before the clinical symptoms become apparent, involves the excessive accumulation of ... ...

Abstract	Alzheimer's disease (AD) is currently constrained by limited clinical treatment options. The initial pathophysiological event, which can be traced back to decades before the clinical symptoms become apparent, involves the excessive accumulation of amyloid-beta (Aβ), a peptide comprised of 40-42 amino acids, in extraneuronal plaques within the brain. Biochemical and histological studies have shown that overaccumulation of Aβ instigates an aberrant escalation in the phosphorylation and secretion of tau, a microtubule-binding axonal protein. The accumulation of hyperphosphorylated tau into intraneuronal neurofibrillary tangles is in turn correlated with microglial dysfunction and reactive astrocytosis, culminating in synaptic dysfunction and neurodegeneration. As neurodegeneration progresses, it gives rise to mild clinical symptoms of AD, which may eventually evolve into overt dementia. Synaptic loss in AD may develop even before tau alteration and in response to possible elevations in soluble oligomeric forms of Aβ associated with early AD. These findings largely rely on post-mortem autopsy examinations, which typically involve a limited number of patients. Over the past decade, a range of fluid biomarkers such as neurogranin, α-synuclein, visinin-like protein 1 (VILIP-1), neuronal pentraxin 2, and β-synuclein, along with positron emission tomography (PET) markers like synaptic vesicle glycoprotein 2A, have been developed. These advancements have facilitated the exploration of how synaptic markers in AD patients correlate with cognitive impairment. However, fluid biomarkers indicating synaptic loss have only been validated in cerebrospinal fluid (CSF), not in plasma, with the exception of VILIP-1. The most promising PET radiotracer, [
Language	English
Publishing date	2024-01-16
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-023-02376-6
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Article ; Online: Digging into the intrinsic capacity concept: Can it be applied to Alzheimer's disease?

López-Ortiz, Susana / Caruso, Giuseppe / Emanuele, Enzo / Menéndez, Héctor / Peñín-Grandes, Saúl / Guerrera, Claudia Savia / Caraci, Filippo / Nisticò, Robert / Lucia, Alejandro / Santos-Lozano, Alejandro / Lista, Simone

Progress in neurobiology

2024 Volume 234, Page(s) 102574

Abstract: Historically, aging research has largely centered on disease pathology rather than promoting healthy aging. The World Health Organization's (WHO) policy framework (2015-2030) underscores the significance of fostering the contributions of older ... ...

Abstract	Historically, aging research has largely centered on disease pathology rather than promoting healthy aging. The World Health Organization's (WHO) policy framework (2015-2030) underscores the significance of fostering the contributions of older individuals to their families, communities, and economies. The WHO has introduced the concept of intrinsic capacity (IC) as a key metric for healthy aging, encompassing five primary domains: locomotion, vitality, sensory, cognitive, and psychological. Past AD research, constrained by methodological limitations, has focused on single outcome measures, sidelining the complexity of the disease. Our current scientific milieu, however, is primed to adopt the IC concept. This is due to three critical considerations: (I) the decline in IC is linked to neurocognitive disorders, including AD, (II) cognition, a key component of IC, is deeply affected in AD, and (III) the cognitive decline associated with AD involves multiple factors and pathophysiological pathways. Our study explores the application of the IC concept to AD patients, offering a comprehensive model that could revolutionize the disease's diagnosis and prognosis. There is a dearth of information on the biological characteristics of IC, which are a result of complex interactions within biological systems. Employing a systems biology approach, integrating omics technologies, could aid in unraveling these interactions and understanding IC from a holistic viewpoint. This comprehensive analysis of IC could be leveraged in clinical settings, equipping healthcare providers to assess AD patients' health status more effectively and devise personalized therapeutic interventions in accordance with the precision medicine paradigm. We aimed to determine whether the IC concept could be extended from older individuals to patients with AD, thereby presenting a model that could significantly enhance the diagnosis and prognosis of this disease.
MeSH term(s)	Humans ; Alzheimer Disease ; Cognitive Dysfunction/diagnosis ; Aging
Language	English
Publishing date	2024-01-22
Publishing country	England
Document type	Journal Article
ZDB-ID	185535-9
ISSN	1873-5118 ; 0301-0082
ISSN (online)	1873-5118
ISSN	0301-0082
DOI	10.1016/j.pneurobio.2024.102574
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Article ; Online: Synaptic degeneration and neurogranin in the pathophysiology of Alzheimer's disease.

Lista, Simone / Hampel, Harald

Expert review of neurotherapeutics

2017 Volume 17, Issue 1, Page(s) 47–57

Abstract: Introduction: Synaptic dysfunction and degeneration are early fundamental pathophysiological characteristics of Alzheimer's disease (AD). In addition, synaptic depletion closely correlates with clinical disease severity. Biomarkers that may track ... ...

Abstract	Introduction: Synaptic dysfunction and degeneration are early fundamental pathophysiological characteristics of Alzheimer's disease (AD). In addition, synaptic depletion closely correlates with clinical disease severity. Biomarkers that may track synaptic dysfunction in AD are eagerly awaited. Areas covered: Here, we reviewed the significance of the post-synaptic protein neurogranin - particularly enriched in dendritic spines - as a biomarker of early synaptic dysfunction in AD. We also examined its role as a marker to predict disease progression. Expert commentary: Current evidence indicates that neurogranin may serve as a mechanism-of-action biomarker aiding the in vivo investigation of AD-related pathophysiological pathways. Its use may support the development of targeted therapeutic interventions tailored to the individual patient, i.e. 'molecularly' targeted therapies, according to the evolving precision medicine paradigm.
MeSH term(s)	Alzheimer Disease/metabolism ; Alzheimer Disease/physiopathology ; Amyloid beta-Peptides/metabolism ; Biomarkers ; Disease Progression ; Humans ; Neurogranin
Chemical Substances	Amyloid beta-Peptides ; Biomarkers ; Neurogranin (132654-77-4)
Language	English
Publishing date	2017-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2112534-X
ISSN	1744-8360 ; 1473-7175
ISSN (online)	1744-8360
ISSN	1473-7175
DOI	10.1080/14737175.2016.1204234
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Article ; Online: Dementia: The rising global tide of cognitive impairment.

Hampel, Harald / Lista, Simone

Nature reviews. Neurology

2016 Volume 12, Issue 3, Page(s) 131–132

MeSH term(s)	Cognitive Dysfunction/epidemiology ; Female ; Humans ; Male
Language	English
Publishing date	2016-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2491514-2
ISSN	1759-4766 ; 1759-4758
ISSN (online)	1759-4766
ISSN	1759-4758
DOI	10.1038/nrneurol.2015.250
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Article ; Online: Time for the systems-level integration of aging: Resilience enhancing strategies to prevent Alzheimer's disease.

Hampel, Harald / Lista, Simone / Neri, Christian / Vergallo, Andrea

Progress in neurobiology

2019 Volume 181, Page(s) 101662

Abstract: Systems biology and systems neurophysiology generate comprehensive mechanistic models of the spatial-temporal evolution of body system networks from physiological to pathophysiological conditions. Alzheimer's disease (AD)-related pathophysiological ... ...

Abstract	Systems biology and systems neurophysiology generate comprehensive mechanistic models of the spatial-temporal evolution of body system networks from physiological to pathophysiological conditions. Alzheimer's disease (AD)-related pathophysiological alterations converge with overexpressed age-related functional decline, i.e. aging, which is induced by genetic- and stochastic time-dependent events. Accumulation of cellular senescence has a casual role in aging-related disease and senotherapeutic drugs have already shown encouraging results for counteracting the detrimental effect of senescence. However, the non-linear complex nature of AD pathophysiology calls for a systems-level integration of aging dynamics, from molecules until large-scale networks. We need a holistic systems-wide comprehensive model of aging which is constituted by a non-linear spatial-temporal weakening of adaptive responses resulting in the activation of compensatory mechanisms that ensure biological robustness, resilience, and finally preserve homeodynamics. After exceeding the threshold of compensated (resilient) aging, a cascade of decompensatory events occurs, ultimately triggering irreversible systems failure that, at some advanced stages, reflect widespread "pathophysiological hallmarks of AD". The gap in the comprehensive understanding of aging, resilience, and AD pathophysiological evolution will be filled through a quantitative, flexible, and integrative modeling approach to detect multiple spatial-temporal patterns and for dissecting causal mechanisms and downstream cascades throughout the aging-AD continuum. Novel technological and conceptual advances, will enable the systems-level integration of aging signatures as well as compensatory mechanisms that provide resilience to early functional decline. This will provide new systems-scaled outcomes and endpoints to map and therapeutically enhance resilience, accomplishing a long-lasting compensated aging.
MeSH term(s)	Aging ; Alzheimer Disease/physiopathology ; Alzheimer Disease/prevention & control ; Humans ; Systems Biology ; Systems Integration
Language	English
Publishing date	2019-07-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	185535-9
ISSN	1873-5118 ; 0301-0082
ISSN (online)	1873-5118
ISSN	0301-0082
DOI	10.1016/j.pneurobio.2019.101662
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Article ; Online: The Alzheimer Precision Medicine Initiative.

Hampel, Harald / Vergallo, Andrea / Perry, George / Lista, Simone

Journal of Alzheimer's disease : JAD

2019 Volume 68, Issue 1, Page(s) 1–24

Abstract: Precision medicine (PM) is an evolving scientific renaissance movement implementing key breakthrough technological and scientific advances to overcome the limitations of traditional symptom- and sign-based phenotypic diagnoses and clinical "one-size-fits- ...

Abstract	Precision medicine (PM) is an evolving scientific renaissance movement implementing key breakthrough technological and scientific advances to overcome the limitations of traditional symptom- and sign-based phenotypic diagnoses and clinical "one-size-fits-all, magic bullet drug development" in these largely heterogeneous target populations. It is a conceptual shift from ineffective treatments for biologically heterogeneous "population averages" to individually-tailored biomarker-guided targeted therapies. PM is defining which therapeutic approach will be the most effective for a specific individual, at a determined disease stage, across multiple medical research fields, including neuroscience, neurology and psychiatry. The launch of the Alzheimer Precision Medicine Initiative (APMI) and its associated cohort program in 2016-facilitated by the academic core coordinating center run by the Sorbonne University Clinical Research Group in Alzheimer Precision Medicine (Sorbonne University GRC n°21 APM)"-is geared at transforming healthcare, conventional clinical diagnostics, and drug development research in Alzheimer's disease. Ever since the commencement of the APMI, the international interdisciplinary research network has introduced groundbreaking translational neuroscience programs on the basis of agnostic exploratory genomics, systems biology, and systems neurophysiology applying innovative "big data science", including breakthrough artificial intelligence-based algorithms. Here, we present the scientific breakthrough advances and the pillars of the theoretical and conceptual development leading to the APMI.
MeSH term(s)	Alzheimer Disease/diagnosis ; Alzheimer Disease/epidemiology ; Alzheimer Disease/therapy ; Biomarkers ; Biomedical Research/methods ; Biomedical Research/trends ; Health Services Needs and Demand/trends ; Humans ; Precision Medicine/methods ; Precision Medicine/trends
Chemical Substances	Biomarkers
Language	English
Publishing date	2019-02-27
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-181121
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