{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T13:42:13Z","timestamp":1792590133429,"version":"4.5.0"},"reference-count":43,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2025,1,27]],"date-time":"2025-01-27T00:00:00Z","timestamp":1737936000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,1,27]],"date-time":"2025-01-27T00:00:00Z","timestamp":1737936000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["alz-journals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Alzheimer's &amp; Dementia"],"published-print":{"date-parts":[[2025,2]]},"abstract":"Abstract<\/jats:title>\n \n INTRODUCTION<\/jats:title>\n The beneficial effects of amyloid beta 1\u201038, or A\u03b2(1\u201038), on Alzheimer's disease (AD) progression in humans in vivo remain controversial. We investigated AD patients' cerebrospinal fluid (CSF) A\u03b2(1\u201038) and AD progression.<\/jats:p>\n <\/jats:sec>\n \n METHODS<\/jats:title>\n Cognitive function and diagnostic change were assessed annually for 3 years in 177 A\u03b2\u2010positive participants with subjective cognitive decline (SCD), mild cognitive impairment (MCI), and dementia from the German Center for Neurodegenerative Diseases (DZNE) longitudinal cognitive impairment and dementia study (DELCODE) cohort using the Mini\u2010Mental State Examination (MMSE), Preclinical Alzheimer's Cognitive Composite (PACC), Clinical Dementia Rating (CDR), and National Institute of Neurological and Communicative Disorders and Stroke\u2013Alzheimer's Disease and Related Disorders Association (NINCDS\u2010ADRDA) criteria. Mixed linear and Cox regression analyses were conducted. CSF was collected at baseline.<\/jats:p>\n <\/jats:sec>\n \n RESULTS<\/jats:title>\n \n Higher A\u03b2(1\u201038) levels were associated with slower PACC (\n p\u00a0<\/jats:italic>\n =\u00a00.001) and slower CDR Sum of Boxes (CDR\u2010SB) (\n p\u00a0<\/jats:italic>\n =\u00a00.002) but not MMSE decline. Including A\u03b2(1\u201040) beyond A\u03b2(1\u201038) in the model confirmed an association of A\u03b2(1\u201038) with slower PACC decline (\n p\u00a0<\/jats:italic>\n =\u00a00.005), but not with CDR\u2010SB or MMSE decline. In addition, higher A\u03b2(1\u201038) baseline levels were associated with a reduced dementia conversion risk.\n <\/jats:p>\n <\/jats:sec>\n \n DISCUSSION<\/jats:title>\n Further research is needed to understand the role of A\u03b2(1\u201038) in AD and its potential for future therapeutic strategies.<\/jats:p>\n <\/jats:sec>\n \n Highlights<\/jats:title>\n \n \n \n This study not only replicates but also extends the existing findings on the role of A\u03b2(1\u201038) (amyloid beta 1\u201038) in Alzheimer's disease (AD) in humans in vivo.<\/jats:p>\n <\/jats:list-item>\n \n Higher baseline A\u03b2(1\u201038) levels were associated with a decreased risk of conversion to AD dementia in subjective cognitive decline (SCD) and mild cognitive impairment (MCI).<\/jats:p>\n <\/jats:list-item>\n \n Different linear\u2010mixed regression models suggest an association between higher A\u03b2(1\u201038) baseline levels and slower Preclinical Alzheimer's Cognitive Composite (PACC) and Clinical Dementia Rating Sum of Boxes (CDR\u2010SB) decline.<\/jats:p>\n <\/jats:list-item>\n \n Including A\u03b2(1\u201040) beyond A\u03b2(1\u201038) in the model confirmed a link between A\u03b2(1\u201038) and PACC decline, but showed no association of A\u03b2(1\u201038) on CDR\u2010SB and Mini\u2010Mental State Examination (MMSE) decline.<\/jats:p>\n <\/jats:list-item>\n \n The impact of short A\u03b2 isoforms in AD progression might have been under\u2010investigated<\/jats:p>\n <\/jats:list-item>\n \n These findings underscore the urgent need for additional research on the role of these shorter A\u03b2 peptides in AD, as they may hold key insights for future therapeutic strategies.<\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/alz.14545","type":"journal-article","created":{"date-parts":[[2025,1,27]],"date-time":"2025-01-27T07:29:33Z","timestamp":1737962973000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Linking higher amyloid beta 1\u201038 (A\u03b2(1\u201038)) levels to reduced Alzheimer's disease progression risk"],"prefix":"10.1002","volume":"21","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5822-1744","authenticated-orcid":false,"given":"Luisa Sophie","family":"Schneider","sequence":"first","affiliation":[{"name":"Department of Psychiatry and Neuroscience Charit\u00e9 \u2013 Universit\u00e4tsmedizin Berlin corporate member of Freie Universit\u00e4t Berlin Humboldt\u2010Universit\u00e4t zu Berlin Berlin Germany"},{"name":"Memory Clinic and Dementia Prevention Center Experimental and Clinical Research Center (ECRC) Berlin Germany"},{"name":"German Center for Neurodegenerative Diseases (DZNE) 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