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Dec 30, 2024 | 
alzres.biomedcentral.com | Maxime Van Egroo |Elise Beckers |Nicholas Ashton |Kaj Blennow |Henrik Zetterberg
ReferencesVan Egroo M, Narbutas J, Chylinski D, Villar González P, Maquet P, Salmon E, et al. Sleep–wake regulation and the hallmarks of the pathogenesis of Alzheimer’s disease. Sleep. 2019;42:1–13. Google Scholar Rigat L, Ouk K, Kramer A, Priller J. Dysfunction of circadian and sleep rhythms in the early stages of Alzheimer’s disease. Acta Physiol. 2023;238:1–13. Google Scholar Winer JR, Morehouse A, Fenton L, Harrison TM, Ayangma L, Reed M, et al.
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Dec 23, 2024 | 
alzres.biomedcentral.com | Georgette Argiris |Muge Akinci |Cleofé Peña-Gómez |Eleni Palpatzis |Marina García-Prat |Mahnaz Shekari | +8 more
ReferencesJack CR, Bennett DA, Blennow K, Carrillo MC, Dunn B, Haeberlein SB, et al. NIA-AA Research Framework: Toward a biological definition of Alzheimer’s disease. Alzheimers Dement. 2018;14(4):535–62. Article PubMed Google Scholar Milà-Alomà M, Suárez-Calvet M, Molinuevo JL. Latest advances in cerebrospinal fluid and blood biomarkers of Alzheimer’s disease. Ther Adv Neurol Disord. 2019;18(12):1756286419888819.
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Oct 28, 2024 | 
nature.com | Stacey L. Kigar |Leonidas Chouliaras |Noah S. Shapiro |George Savulich |Kaj Blennow |Henrik Zetterberg | +2 more
AbstractThe innate immune system plays an integral role in the progression of many neurodegenerative diseases. In addition to central innate immune cells (e.g., microglia), peripheral innate immune cells (e.g., blood monocytes, natural killer cells, and dendritic cells) may also differ in these conditions. However, the characterization of peripheral innate immune cell types across different neurodegenerative diseases remains incomplete.
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Oct 16, 2024 | 
biorxiv.org | Katharina Waury |Hlin Kvartsberg |Henrik Zetterberg |Kaj Blennow
AbstractAntibodies are indispensable in laboratory and clinical applications due to their high specificity and affinity for protein antigens. However, selecting the right protein fragments as immunogens for antibody production remains challenging. Leveraging the Human Protein Atlas, this study systematically evaluates immunogen properties aiming to identify key factors that influence their suitability.
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Oct 11, 2024 | 
biorxiv.org | Katharina Waury |Hlin Kvartsberg |Henrik Zetterberg |Kaj Blennow
AbstractAntibodies are indispensable in laboratory and clinical applications due to their high specificity and affinity for protein antigens. However, selecting the right protein fragments as immunogens for antibody production remains challenging. Leveraging the Human Protein Atlas, this study systematically evaluates immunogen properties aiming to identify key factors that influence their suitability.
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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 2, 2024 | 
nature.com | Robert Sigström |Andreas Göteson |Axel Nordenskjöld |Kaj Blennow |Henrik Zetterberg
AbstractDespite electroconvulsive therapy (ECT) being recognized as an effective treatment for major depressive episodes (MDE), its application is subject to controversy due to concerns over cognitive side effects. The pathophysiology of these side effects is not well understood. Here, we examined the effects of ECT on blood-based biomarkers of neuronal injury and astrocytic reactivity. Participants with a major depressive episode (N = 99) underwent acute ECT.
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Sep 8, 2024 | 
nature.com | Makrina Daniilidou |Henrik Zetterberg |Kaj Blennow
AbstractCortisol dysregulation, neuroinflammation, and cerebrovascular dysfunction are biological processes that have been separately shown to be affected in Alzheimer’s disease (AD). Here, we aimed to identify biomarker signatures reflecting these pathways in 108 memory clinic patients with subjective cognitive decline (SCD, N = 40), mild cognitive impairment (MCI, N = 39), and AD (N = 29).
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May 31, 2024 | 
lakartidningen.se | Kaj Blennow |Oskar Hansson
Vi har bevittnat imponerande framsteg inom den kliniska forskningen kring Alzheimers sjukdom, vilka gett en detaljerad kunskap om den molekylära patologi som karakteriserar sjukdomen. Dessa patofysiologiska processer innefattar i korthet aggregering av amyloid-beta (Aβ) till Aβ-innehållande plack, fosforylering och aggregering av tau-protein med bildning av neurofibriller i nervcellernas cytoplasma och dystrofiska neuriter som omger placken, samt degeneration av nervceller och deras synapser [1].
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May 3, 2024 | 
nature.com | Gleb Bezgin |Thomas K. Karikari |Henrik Zetterberg |Kaj Blennow |Pedro Rosa-Neto
AbstractNeuronal dysfunction and cognitive deterioration in Alzheimer’s disease (AD) are likely caused by multiple pathophysiological factors. However, mechanistic evidence in humans remains scarce, requiring improved non-invasive techniques and integrative models.
