Ainara Estanga

ORCID: 0000-0002-6616-314X
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About
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Research Areas
  • Dementia and Cognitive Impairment Research
  • Alzheimer's disease research and treatments
  • Parkinson's Disease Mechanisms and Treatments
  • Frailty in Older Adults
  • Neurobiology of Language and Bilingualism
  • Nutritional Studies and Diet
  • Advanced Neuroimaging Techniques and Applications
  • Memory and Neural Mechanisms
  • Functional Brain Connectivity Studies
  • Aging, Health, and Disability
  • Emotion and Mood Recognition
  • Cancer-related cognitive impairment studies
  • Ginkgo biloba and Cashew Applications
  • Neurological diseases and metabolism
  • Genetic Neurodegenerative Diseases
  • Infant Health and Development
  • Metabolomics and Mass Spectrometry Studies
  • Amyotrophic Lateral Sclerosis Research
  • Cholesterol and Lipid Metabolism
  • Traditional Chinese Medicine Studies
  • Health, Environment, Cognitive Aging
  • Health Systems, Economic Evaluations, Quality of Life
  • Radiomics and Machine Learning in Medical Imaging
  • Spectroscopy Techniques in Biomedical and Chemical Research
  • Brain Tumor Detection and Classification

Fundacion CITA Alzheimer
2016-2025

Osakidetza
2010-2024

Universidad de Deusto
2024

Amyloidosis Foundation
2023

Mayo Clinic
2019

WinnMed
2019

Research Network (United States)
2018

Biogipuzkoa Health Research Institute
2009-2018

Karolinska University Hospital
2018

Karolinska Institutet
2018

Abstract Introduction Cortical mean diffusivity (MD) and free water fraction (FW) changes are proposed biomarkers for Alzheimer's disease (AD). Methods We included healthy control subjects (N = 254), mild cognitive impairment 41), AD dementia 31) patients. Participants underwent a lumbar puncture 3 T magnetic resonance imaging. Healthy were classified following National Institute on Aging‐Alzheimer's Association stages (stage 0, N 220; stage 1, 25; 2/3, 9). assessed the cortical MD, FW,...

10.1016/j.jalz.2017.09.013 article EN Alzheimer s & Dementia 2017-10-25

<h3>Objective:</h3> To investigate CSF markers involved in amyloid precursor protein processing, neuronal damage, and neuroinflammation the preclinical stages of Alzheimer disease (AD) participants with suspected non-Alzheimer pathology (SNAP). <h3>Methods:</h3> We collected from 266 cognitively normal volunteers participating a cross-sectional multicenter study (the SIGNAL study) to processing (Aβ42, sAPPβ, β-secretase activity), damage (total-tau [t-tau], phospho-tau [p-tau]), (YKL-40)....

10.1212/wnl.0000000000001859 article EN Neurology 2015-07-16

Abstract Background GOIZ ZAINDU (“caring early” in Basque) is a pilot study to adapt the Finnish Geriatric Intervention Study Prevent Cognitive Impairment and Disability (FINGER) methodology Basque population evaluate feasibility adherence FINGER-like multidomain intervention program. Additional aims included assessment of efficacy on cognition data collection design large trial. Method 1-year, randomized, controlled trial persons aged 60+ years, with Cardiovascular Risk Factors, Aging...

10.1186/s13195-024-01393-z article EN cc-by Alzheimer s Research & Therapy 2024-02-27

Objective: Nowadays proper detection of cognitive impairment has become a challenge for the scientific community. Alzheimer's Disease (AD), most common cause dementia, high prevalence that is increasing at fast pace towards epidemic level. In not-so-distant future this fact could have dramatic social and economic impact. scenario, an early accurate diagnosis AD help to decrease its effects on patients, relatives society. Over last decades there been useful advances not only in classic...

10.2174/1567205014666171120143800 article EN Current Alzheimer Research 2017-11-22

We aimed to determine whether cognitively unimpaired (CU) amyloid- beta-positive (Aβ+) individuals display decreased practice effects on serial neuropsychological testing. included 209 CU participants from three research centers, 157 Aβ- controls and 52 Aβ+ individuals. Participants underwent assessment at baseline annually during a 2-year follow-up. used linear mixed-effects models analyze cognitive change over time between the two groups, including baseline, amyloid status, their...

10.1002/alz.70016 article EN cc-by-nc Alzheimer s & Dementia 2025-03-01

Background: Aging is a well-established independent risk factor for both cognitive impairment and sleep disorders, including obstructive apnea (OSA), modifiable yet underrecognized condition. OSA has been implicated in biological mechanisms contributing to Alzheimer’s disease, amyloid-β accumulation, tau phosphorylation, neuroinflammation. This underscores the need optimize diagnosis individuals with an increased of dementia. Methods: cross-sectional observational study enrolled adults aged...

10.3390/jcm14082607 article EN Journal of Clinical Medicine 2025-04-10

Gerstmann-Sträussler-Scheinker (GSS) disease is a prion associated with protein gene (PRNP) mutations. We report novel PRNP mutation (Y218N) GSS in pathologically confirmed case and two other affected family members. The clinical features of these cases met criteria for possible Alzheimer frontotemporal dementia. Neuropathologic analysis revealed deposition proteinase K-resistant (PrP(res)), widespread hyperphosphorylated tau pathology, abnormal accumulation mitochondria the vicinity PrP...

10.1097/nen.0b013e3181e85737 article EN Journal of Neuropathology & Experimental Neurology 2010-07-07

Background: Dementia and mild cognitive impairment (MCI) are frequent in Parkinson's disease (PD). Deficits some tests considered risk factors for dementia PD. However, how deficits progress aged long-lasting non-

10.3233/jpd-140398 article EN Journal of Parkinson s Disease 2014-01-01

Background The objective of this study was to motor and nonmotor symptoms striatal dopaminergic denervation, as well the relationship between them, in a cohort asymptomatic relatives patients with Parkinson's disease (PD) R1441G-leucine-rich repeat kinase 2 mutation. Methods Asymptomatic PD mutation were tested for presence evaluated striatal, putamenal, caudate transporters using 123I-2β-carbomethoxy-3β-(4-iodophenyl)-N-(3-fluoropropyl)-nortropane single-photon emission computed tomography...

10.1002/mds.26478 article EN Movement Disorders 2015-12-21

To investigate the cognitive profile of healthy individuals with increased Cardiovascular Risk Factors, Aging and Dementia (CAIDE) dementia risk score to explore whether this association is related vascular burden CSF biomarkers amyloidosis neurodegeneration.Cognitively normal participants (mean age 57.6 years) from Gipuzkoa Alzheimer Project study were classified as having high (HR; n = 82) or low (LR; 293) for according a CAIDE cutoff 9. Cognitive composites compared between groups. We...

10.1212/wnl.0000000000005824 article EN Neurology 2018-06-13

We investigated whether amyloid-β (Aβ) and tau affected cognition in cognitively normal (CN) individuals, norms for neuropsychological tests based on biomarker-negative individuals would improve early detection of dementia. included 907 CN from 8 European cohorts the Alzheimer's disease Neuroimaging Initiative. All were aged above 40, had Aβ status data available. Linear mixed models used to assess associations with five assessing memory (immediate delayed recall Auditory Verbal Learning...

10.3389/fnagi.2018.00193 article EN cc-by Frontiers in Aging Neuroscience 2018-06-25

Mutations in the progranulin gene (PGRN) are a major cause of frontotemporal lobar degeneration with tau-negative and ubiquitin-positive neuronal inclusions. Most previous studies aimed at characterizing clinical neuropsychological phenotype PGRN mutation carriers included patients different mutations, assuming that common proposed pathogenetic mechanism haploinsufficiency will lead to comparable phenotype.We studied 21 single pathogenic splicing (c.709-1G>A) same tertiary referral center...

10.1212/wnl.0b013e3181bd82a7 article EN Neurology 2009-10-26

An inverse relationship between Parkinson's disease (PD) and cancer has been described. However, the association cancers genetic forms of PD, in particular R1441G mutation LRRK2 gene, is not well known. The objective this work was to analyze prevalence PD patients with or G2019S mutations LRRK2, idiopathic (iPD). A total 732 (70 25 carriers mutations, respectively), 177 controls, were linked using a population-based registry Spanish province Gipuzkoa. Cancer significantly higher PD-G2019S...

10.1002/mds.25778 article EN Movement Disorders 2013-12-19

Abstract Introduction Amyloid plaque deposition in the brain is an early pathological change Alzheimer's disease (AD), causing disrupted synaptic connections. Brain network disruptions AD have been demonstrated with eigenvector centrality (EC), a measure that identifies central regions within networks. Carrying apolipoprotein (APOE)‐ε4 allele genetic risk for AD, associated increased amyloid deposition. We studied whether APOE‐ε4 carriership EC cognitively normal individuals. Methods A total...

10.1002/brb3.1080 article EN cc-by Brain and Behavior 2018-08-22

Abstract Mutations in the progranulin (PGRN) gene have been identified as a cause of frontotemporal dementia (FTD). However, little is known about neuropsychological abilities asymptomatic carriers these mutations. The aim study was to assess cognitive functioning c.709-1G&gt;A PGRN mutation carriers. We hypothesized that poorer performance could be present before development clinically significant FTD symptoms. Thirty-two first-degree relatives patients carrying served participants,...

10.1017/s1355617712000823 article EN Journal of the International Neuropsychological Society 2012-11-01

We employed a highly demanding experimental associative learning test (the AFE-T) to explore memory functioning in Preclinical Alzheimer's Disease stage 1 (PreAD-1) and 2 (PreAD-2). The task consisted the of unknown object/name pairs our comprehensive setup allowed analysi s curves, immediate recall, long-term forgetting rates at one week, three months, six relearning curves. Forty-nine cognitively healthy subjects were included classified according presence or absence abnormal CSF...

10.3233/jad-161173 article EN Journal of Alzheimer s Disease 2017-05-09
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