9 results on '"Villarejo-Galende, Alberto"'
Search Results
2. Charting Alzheimer's Disease and Dementia: Epidemiological Insights, Risk Factors and Prevention Pathways.
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Contador, Israel, Buch-Vicente, Bárbara, del Ser, Teodoro, Llamas-Velasco, Sara, Villarejo-Galende, Alberto, Benito-León, Julián, and Bermejo-Pareja, Félix
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ALZHEIMER'S disease ,HEALTH policy ,COGNITION disorders ,SCIENTIFIC literature ,DEMENTIA ,CEREBRAL amyloid angiopathy - Abstract
Alzheimer's disease (AD), the most common cause of dementia, is a complex and multifactorial condition without cure at present. The latest treatments, based on anti-amyloid monoclonal antibodies, have only a modest effect in reducing the progression of cognitive decline in AD, whereas the possibility of preventing AD has become a crucial area of research. In fact, recent studies have observed a decrease in dementia incidence in developed regions such as the US and Europe. However, these trends have not been mirrored in non-Western countries (Japan or China), and the contributing factors of this reduction remain unclear. The Lancet Commission has delineated a constrained classification of 12 risk factors across different life stages. Nevertheless, the scientific literature has pointed to over 200 factors—including sociodemographic, medical, psychological, and sociocultural conditions—related to the development of dementia/AD. This narrative review aims to synthesize the risk/protective factors of dementia/AD. Essentially, we found that risk/protective factors vary between individuals and populations, complicating the creation of a unified prevention strategy. Moreover, dementia/AD explanatory mechanisms involve a diverse array of genetic and environmental factors that interact from the early stages of life. In the future, studies across different population-based cohorts are essential to validate risk/protective factors of dementia. This evidence would help develop public health policies to decrease the incidence of dementia. [ABSTRACT FROM AUTHOR]
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- 2024
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3. Annexin A5 prevents amyloid-β-induced toxicity in choroid plexus : implication for Alzheimer's disease
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Bartolome, Fernando, Krzyzanowska, Agnieszka, de la Cueva, Macarena, Pascual, Consuelo, Antequera, Desiree, Spuch, Carlos, Villarejo-Galende, Alberto, Rábano, Alberto, Fortea, Juan, Alcolea, Daniel, Lleó, Alberto, Ferrer, Isidro, Hardy, John, Abramov, Andrey Y., Carro, Eva, and Universitat Autònoma de Barcelona
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Male ,Proteomics ,Cell death in the nervous system ,lcsh:Medicine ,Apoptosis ,Annexin A5 ,lcsh:Science ,Cells, Cultured ,Aged, 80 and over ,Neurons ,Multidisciplinary ,Middle Aged ,Alzheimer's disease ,Blood-Brain Barrier ,Toxicity ,Choroid plexus ,Female ,medicine.medical_specialty ,Programmed cell death ,2411 Fisiología Humana ,Bioenergetics ,Article ,Protein metabolism ,Alzheimer Disease ,Internal medicine ,medicine ,Extracellular ,Autophagy ,Animals ,Humans ,Cognitive Dysfunction ,Rats, Wistar ,Aged ,Amyloid beta-Peptides ,business.industry ,lcsh:R ,Rats ,Endocrinology ,Malaltia d'Alzheimer ,Cell culture ,Choroid Plexus ,lcsh:Q ,Calcium ,Metabolisme de proteïnes ,business ,Neurological disorders - Abstract
In Alzheimer’s disease (AD) amyloid-β (Aβ) deposits may cause impairments in choroid plexus, a specialised brain structure which forms the blood–cerebrospinal fluid (CSF) barrier. We previously carried out a mass proteomic-based study in choroid plexus from AD patients and we found several differentially regulated proteins compared with healthy subjects. One of these proteins, annexin A5, was previously demonstrated implicated in blocking Aβ-induced cytotoxicity in neuronal cell cultures. Here, we investigated the effects of annexin A5 on Aβ toxicity in choroid plexus. We used choroid plexus tissue samples and CSF from mild cognitive impairment (MCI) and AD patients to analyse Aβ accumulation, cell death and annexin A5 levels compared with control subjects. Choroid plexus cell cultures from rats were used to analyse annexin A5 effects on Aβ-induced cytotoxicity. AD choroid plexus exhibited progressive reduction of annexin A5 levels along with progressive increased Aβ accumulation and cell death as disease stage was higher. On the other hand, annexin A5 levels in CSF from patients were found progressively increased as the disease stage increased in severity. In choroid plexus primary cultures, Aβ administration reduced endogenous annexin A5 levels in a time-course dependent manner and simultaneously increased annexin A5 levels in extracellular medium. Annexin A5 addition to choroid plexus cell cultures restored the Aβ-induced impairments on autophagy flux and apoptosis in a calcium-dependent manner. We propose that annexin A5 would exert a protective role in choroid plexus and this protection is lost as Aβ accumulates with the disease progression. Then, brain protection against further toxic insults would be jeopardised. Instituto de Salud Carlos III | Ref. FIS2015/00780 Instituto de Salud Carlos III | Ref. PI18/00118 Instituto de Salud Carlos III | Ref. PI2016/01 Comunidad de Madrid | Ref. S2017/BMD-3700 Fundación Ramón Areces | Ref. CIVP16A1825
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- 2020
4. Early diagnosis of mild cognitive impairment and Alzheimer's disease based on salivary lactoferrin
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Carro, Eva, Bartolomé, Fernando, Bermejo-Pareja, Félix, Villarejo-Galende, Alberto, Molina, José Antonio, Ortiz, Pablo, Rábano, Alberto, Cantero, José Luis, Orive, Gorka, Bermejo‐Pareja, Félix, Villarejo‐Galende, Alberto, and Calero, Miguel
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0301 basic medicine ,Oncology ,Pathology ,medicine.medical_specialty ,Saliva ,Neurology ,Amyloid ,Disease ,lcsh:Geriatrics ,lcsh:RC346-429 ,03 medical and health sciences ,0302 clinical medicine ,Cerebrospinal fluid ,Internal medicine ,Diagnosis ,Noninvasive biomarker ,medicine ,Cognitive decline ,Noninvasive biomarkers ,lcsh:Neurology. Diseases of the nervous system ,Diagnostic Assessment & Prognosis ,biology ,Lactoferrin ,Mild cognitive impairment ,Alzheimer's disease ,lcsh:RC952-954.6 ,Psychiatry and Mental health ,030104 developmental biology ,biology.protein ,Biomarker (medicine) ,Dementia ,Neurology (clinical) ,Psychology ,Alzheimer’s disease ,030217 neurology & neurosurgery - Abstract
The Alzheimer's disease (AD) process is likely initiated many years before clinical onset. Biomarkers of preclinical disease are critical for the development of disease-modifying or even preventative therapies. Current biomarkers for early disease, including cerebrospinal fluid tau and amyloid β (Aβ) levels, structural and functional magnetic resonance imaging, and the use of brain amyloid imaging, are limited because they are very invasive or expensive. Noninvasive biomarkers may be a more accessible alternative, but none can currently detect preclinical AD with the required sensitivity and specificity. Here, we show a novel, straight-forward, and noninvasive approach for assessment of early stages of cognitive decline. Salivary samples from cases of amnestic mild cognitive impairment (aMCI) and AD, and neurology controls were analyzed. We have discovered and validated a new single saliva biomarker, lactoferrin, which in our cross-sectional investigation perfectly discriminates clinically diagnosed aMCI and AD patients from a cognitively healthy control group. The accuracy for AD diagnosis shown by salivary lactoferrin was greater than that obtained from core cerebrospinal fluid (CSF) biomarkers, including total tau and CSF Aβ42. Furthermore, salivary lactoferrin can be used for population screening and for identifying those underdiagnosed subjects with very early stages of mild cognitive impairment and AD. This biomarker may offer new insights in the early diagnostics for AD. The authors are grateful to Juan Carlos del Castillo who participated in the promotion of this study. The authors specially thank Raquel Cobos, Consuelo Pascual, Desiree Antequera, Jose Javier Aguirre, Belén González-Lahera, Alicia Maroto, and Ana B. Pastor for their helpful support and technical assistance. The authors want to particularly acknowledge the patients enrolled in this study for their participation and the Biobanco imas12 in Hospital 12 de Octubre integrated in the in Spanish Hospital Biobanks Network (RetBioH; www.redbiobancos.es). Biobank is supported by Instituto de Salud Carlos III. This work was supported by a grant from GEROA Diagnostics (grant 2015/82). Sí
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- 2017
5. Texture-Based Analysis of 18 F-Labeled Amyloid PET Brain Images.
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Seiffert, Alexander P., Gómez-Grande, Adolfo, Milara, Eva, Llamas-Velasco, Sara, Villarejo-Galende, Alberto, Gómez, Enrique J., Sánchez-González, Patricia, and Bueno, Gloria
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BRAIN imaging ,AMYLOID ,RECEIVER operating characteristic curves ,POSITRON emission tomography ,ALZHEIMER'S disease ,BRAIN-computer interfaces ,LABELS ,DIAGNOSIS - Abstract
Amyloid positron emission tomography (PET) brain imaging with radiotracers like [
18 F]florbetapir (FBP) or [18 F]flutemetamol (FMM) is frequently used for the diagnosis of Alzheimer's disease. Quantitative analysis is usually performed with standardized uptake value ratios (SUVR), which are calculated by normalizing to a reference region. However, the reference region could present high variability in longitudinal studies. Texture features based on the grey-level co-occurrence matrix, also called Haralick features (HF), are evaluated in this study to discriminate between amyloid-positive and negative cases. A retrospective study cohort of 66 patients with amyloid PET images (30 [18 F]FBP and 36 [18 F]FMM) was selected and SUVRs and 6 HFs were extracted from 13 cortical volumes of interest. Mann–Whitney U-tests were performed to analyze differences of the features between amyloid positive and negative cases. Receiver operating characteristic (ROC) curves were computed and their area under the curve (AUC) was calculated to study the discriminatory capability of the features. SUVR proved to be the most significant feature among all tests with AUCs between 0.692 and 0.989. All HFs except correlation also showed good performance. AUCs of up to 0.949 were obtained with the HFs. These results suggest the potential use of texture features for the classification of amyloid PET images. [ABSTRACT FROM AUTHOR]- Published
- 2021
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6. Non-steroidal anti-inflammatory drugs use in older adults decreases risk of Alzheimer’s disease mortality.
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Benito-León, Julián, Contador, Israel, Vega, Saturio, Villarejo-Galende, Alberto, and Bermejo-Pareja, Félix
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ALZHEIMER'S disease ,OLDER people ,ANTI-inflammatory agents ,DRUG abuse ,COMORBIDITY ,MORTALITY - Abstract
Alzheimer disease (AD) mortality risk in a large cohort of subjects treated or not with non-steroidal anti-inflammatory drugs (NSAIDs) is unknown. Our objective was to determine whether NSAIDs use is associated with decreased risk of AD mortality. In this prospective, population-based study (Neurological Disorders in Central Spain [NEDICES]) of 5,072 people without AD (aged 65 years and older), sociodemographic, comorbidity factors, and current medications were recorded at baseline. Community-dwelling older adults were followed for a median of 12.7 years, after which the death certificates of deceased participants were examined. 2,672 (52.7%) of 5,072 participants died, including 504 (18.9%) NSAIDs users and 2,168 (81.1%) non-users. Of the 2,672 deceased participants, 113 (4.2%) had AD as a cause of death (8 [1.6%] among NSAIDs users and 105 [4.8%] among non-users, chi-square = 10.70, p = 0.001). In an unadjusted Cox model, risk of AD mortality was decreased in NSAIDs users (hazard ratio [HR] for AD mortality = 0.35, 95% confidence interval [CI] 0.17–0.72, p = 0.004) when compared to non-users. After adjusting for numerous demographic factors and co-morbidities, the HR for AD mortality in NSAIDs users was 0.29, 95% CI 0.12–0.73, p = 0.009. Stratified analyses showed a significantly decreased risk of AD mortality with aspirin, whereas non-aspirin NSAIDs only showed a statistical trend toward significance in the adjusted Cox regression models. NSAIDs use was associated with 71% decreased risk of AD mortality in older adults. Our results support the hypothesis that NSAIDs use is a protective factor of developing AD. [ABSTRACT FROM AUTHOR]
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- 2019
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7. Increased YKL-40 but Not C-Reactive Protein Levels in Patients with Alzheimer's Disease.
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Blanco-Palmero, Víctor Antonio, Rubio-Fernández, Marcos, Antequera, Desireé, Villarejo-Galende, Alberto, Molina, José Antonio, Ferrer, Isidro, Bartolome, Fernando, and Carro, Eva
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ALZHEIMER'S patients ,C-reactive protein ,PREFRONTAL cortex ,OLDER patients ,MILD cognitive impairment - Abstract
Neuroinflammation is a common feature in Alzheimer's (AD) and Parkinson's (PD) disease. In the last few decades, a testable hypothesis was proposed that protein-unfolding events might occur due to neuroinflammatory cascades involving alterations in the crosstalk between glial cells and neurons. Here, we tried to clarify the pattern of two of the most promising biomarkers of neuroinflammation in cerebrospinal fluid (CSF) in AD and PD. This study included cognitively unimpaired elderly patients, patients with mild cognitive impairment, patients with AD dementia, and patients with PD. CSF samples were analyzed for YKL-40 and C-reactive protein (CRP). We found that CSF YKL-40 levels were significantly increased only in dementia stages of AD. Additionally, increased YKL-40 levels were found in the cerebral orbitofrontal cortex from AD patients in agreement with augmented astrogliosis. Our study confirms that these biomarkers of neuroinflammation are differently detected in CSF from AD and PD patients. [ABSTRACT FROM AUTHOR]
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- 2021
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8. High Correlation of Static First-Minute-Frame (FMF) PET Imaging after 18 F-Labeled Amyloid Tracer Injection with [ 18 F]FDG PET Imaging.
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Seiffert, Alexander P., Gómez-Grande, Adolfo, Villarejo-Galende, Alberto, González-Sánchez, Marta, Bueno, Héctor, Gómez, Enrique J., and Sánchez-González, Patricia
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AMYLOID ,PEARSON correlation (Statistics) ,RADIOACTIVE tracers - Abstract
Dynamic early-phase PET images acquired with radiotracers binding to fibrillar amyloid-beta (Aβ) have shown to correlate with [
18 F]fluorodeoxyglucose (FDG) PET images and provide perfusion-like information. Perfusion information of static PET scans acquired during the first minute after radiotracer injection (FMF, first-minute-frame) is compared to [18 F]FDG PET images. FMFs of 60 patients acquired with [18 F]florbetapir (FBP), [18 F]flutemetamol (FMM), and [18 F]florbetaben (FBB) are compared to [18 F]FDG PET images. Regional standardized uptake value ratios (SUVR) are directly compared and intrapatient Pearson's correlation coefficients are calculated to evaluate the correlation of FMFs to their corresponding [18 F]FDG PET images. Additionally, regional interpatient correlations are calculated. The intensity profiles of mean SUVRs among the study cohort (r = 0.98, p < 0.001) and intrapatient analyses show strong correlations between FMFs and [18 F]FDG PET images (r = 0.93 ± 0.05). Regional VOI-based analyses also result in high correlation coefficients. The FMF shows similar information to the cerebral metabolic patterns obtained by [18 F]FDG PET imaging. Therefore, it could be an alternative to the dynamic imaging of early phase amyloid PET and be used as an additional neurodegeneration biomarker in amyloid PET studies in routine clinical practice while being acquired at the same time as amyloid PET images. [ABSTRACT FROM AUTHOR]- Published
- 2021
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9. Kynurenic Acid Levels are Increased in the CSF of Alzheimer's Disease Patients.
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González-Sánchez, Marta, Jiménez, Javier, Narváez, Arantzazu, Antequera, Desiree, Llamas-Velasco, Sara, Herrero-San Martín, Alejandro, Molina Arjona, Jose Antonio, López de Munain, Adolfo, Lleó Bisa, Alberto, Marco, M.-Pilar, Rodríguez-Núñez, Montserrat, Pérez-Martínez, David Andrés, Villarejo-Galende, Alberto, Bartolome, Fernando, Domínguez, Elena, and Carro, Eva
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ALZHEIMER'S patients ,CEREBROSPINAL fluid examination ,AMYOTROPHIC lateral sclerosis ,CEREBROSPINAL fluid ,PROGRESSIVE supranuclear palsy ,ALZHEIMER'S disease ,FRONTOTEMPORAL dementia - Abstract
Kynurenic acid (KYNA) is a product of the tryptophan (TRP) metabolism via the kynurenine pathway (KP). This pathway is activated in neurodegenerative disorders, such as Alzheimer´s disease (AD). KYNA is primarily produced by astrocytes and is considered neuroprotective. Thus, altered KYNA levels may suggest an inflammatory response. Very recently, significant increases in KYNA levels were reported in cerebrospinal fluid (CSF) from AD patients compared with normal controls. In this study, we assessed the accuracy of KYNA in CSF for the classification of patients with AD, cognitively healthy controls, and patients with a variety of other neurodegenerative diseases, including frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), and progressive supranuclear palsy (PSP). Averaged KYNA concentration in CSF was higher in patients with AD when compared with healthy subjects and with all the other differentially diagnosed groups. There were no significant differences in KYNA levels in CSF between any other neurodegenerative groups and controls. These results suggest a specific increase in KYNA concentration in CSF from AD patients not seen in other neurodegenerative diseases. [ABSTRACT FROM AUTHOR]
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- 2020
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