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Nov 14, 2024 | 
bpspsychub.onlinelibrary.wiley.com | Joel Simrén |Nicholas Ashton |Marc Suárez-Calvet |Henrik Zetterberg
Recent developments in fluid and imaging biomarkers that reflect the key pathological hallmarks of Alzheimer's disease (AD)—deposits of extracellular amyloid-β (Aβ) and intracellular tau proteins—have transformed the perception of the disease in living individuals from a clinical syndrome to a biological continuum that begins prior to the onset of symptoms (Scheltens et al., 2021).
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Oct 8, 2024 | 
nature.com | Clara Vila-Castelar |Eleni Palpatzis |Kaj Blennow |Henrik Zetterberg |Juan Domingo Gispert |Marc Suárez-Calvet | +2 more
AbstractGlial reactivity may contribute to sex/gender differences in Alzheimer’s disease (AD) pathophysiology. Here, we investigated the differential effect of cerebrospinal fluid (CSF) glial markers on AD pathology and neurodegeneration by sex/gender among cognitively unimpaired older adults at increased risk of developing AD.
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Oct 8, 2024 | 
biorxiv.org | Eva Borras |Federica Anastasi |Olga Pastor |Marc Suárez-Calvet
AbstractCerebrospinal fluid (CSF) is a valuable liquid biopsy for identifying protein biomarkers in neurological diseases, yet its proteome profiling faces challenges due to the large dynamic range of protein abundances. In this study, we assessed the effectiveness of a commercial enrichment strategy, initially developed for plasma samples, in enhancing the detection of low-abundance proteins in human CSF.
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Jul 18, 2024 | 
nature.com | Juan Fortea |Daniel Alcolea |Olivia Belbin |Oriol Dols-Icardo |Laura Videla |Marc Suárez-Calvet | +4 more
replying to C. Pappalettera et al. Nat. Med. https://doi.org/10.1038/s41591-024-03158-5 (2024)Pappalettera et al.1 raise important points concerning our recent publication on APOE4 homozygotes2, specifically about the definition of Alzheimer’s disease (AD), resilience factors, and the ethical implications of diagnosing asymptomatic individuals.
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Jun 17, 2024 | 
nature.com | Juan Fortea |Jordi Pegueroles |Daniel Alcolea |Olivia Belbin |Oriol Dols-Icardo |Laura Videla | +5 more
Correction to: Nature Medicine https://doi.org/10.1038/s41591-024-02931-w, published online 6 May 2024In the version of the article initially published, the title of Fig. 4 read “APOE3 homozygotes” and has now been amended to “APOE4 homozygotes” in the HTML and PDF versions of the article. About this articleFortea, J., Pegueroles, J., Alcolea, D. et al. Publisher Correction: APOE4 homozygosity represents a distinct genetic form of Alzheimer’s disease. Nat Med (2024).
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Jun 12, 2024 | 
nature.com | Suzanne Schindler |Marc Suárez-Calvet |Ara Khachaturian |Michelle M. Mielke |Yan Hu |Soeren Mattke
AbstractAnti-amyloid treatments for early symptomatic Alzheimer disease have recently become clinically available in some countries, which has greatly increased the need for biomarker confirmation of amyloid pathology. Blood biomarker (BBM) tests for amyloid pathology are more acceptable, accessible and scalable than amyloid PET or cerebrospinal fluid (CSF) tests, but have highly variable levels of performance.
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May 6, 2024 | 
nature.com | Juan Fortea |Jordi Pegueroles |Daniel Alcolea |Olivia Belbin |Oriol Dols-Icardo |Laura Videla | +5 more
AbstractThis study aimed to evaluate the impact of APOE4 homozygosity on Alzheimer’s disease (AD) by examining its clinical, pathological and biomarker changes to see whether APOE4 homozygotes constitute a distinct, genetically determined form of AD. Data from the National Alzheimer’s Coordinating Center and five large cohorts with AD biomarkers were analyzed. The analysis included 3,297 individuals for the pathological study and 10,039 for the clinical study.
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Apr 4, 2024 | 
nature.com | Fernando Gonzalez-Ortiz |Jose Celso Contador |Geir Bråthen |Przemyslaw R. Kac |Johanna Nilsson |Kathleen Hayden | +5 more
AbstractStaging amyloid-beta (Aβ) pathophysiology according to the intensity of neurodegeneration could identify individuals at risk for cognitive decline in Alzheimer’s disease (AD). In blood, phosphorylated tau (p-tau) associates with Aβ pathophysiology but an AD-type neurodegeneration biomarker has been lacking.
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Apr 4, 2024 | nature.com | Fernando Gonzalez-Ortiz |Jose Celso Contador |Geir Bråthen |Przemyslaw R. Kac |Johanna Nilsson |Kathleen Hayden | +5 more
AbstractStaging amyloid-beta (Aβ) pathophysiology according to the intensity of neurodegeneration could identify individuals at risk for cognitive decline in Alzheimer’s disease (AD). In blood, phosphorylated tau (p-tau) associates with Aβ pathophysiology but an AD-type neurodegeneration biomarker has been lacking.
