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000277323 1001_ $$0P:(DE-2719)9002878$$aSchneider, Luisa Sophie$$b0
000277323 245__ $$aLinking higher amyloid beta 1-38 (Aβ(1-38)) levels to reduced Alzheimer's disease progression risk.
000277323 260__ $$aHoboken, NJ$$bWiley$$c2025
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000277323 520__ $$aThe beneficial effects of amyloid beta 1-38, or Aβ(1-38), on Alzheimer's disease (AD) progression in humans in vivo remain controversial. We investigated AD patients' cerebrospinal fluid (CSF) Aβ(1-38) and AD progression.Cognitive function and diagnostic change were assessed annually for 3 years in 177 Aβ-positive 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-Mental State Examination (MMSE), Preclinical Alzheimer's Cognitive Composite (PACC), Clinical Dementia Rating (CDR), and National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA) criteria. Mixed linear and Cox regression analyses were conducted. CSF was collected at baseline.Higher Aβ(1-38) levels were associated with slower PACC (p = 0.001) and slower CDR Sum of Boxes (CDR-SB) (p = 0.002) but not MMSE decline. Including Aβ(1-40) beyond Aβ(1-38) in the model confirmed an association of Aβ(1-38) with slower PACC decline (p = 0.005), but not with CDR-SB or MMSE decline. In addition, higher Aβ(1-38) baseline levels were associated with a reduced dementia conversion risk.Further research is needed to understand the role of Aβ(1-38) in AD and its potential for future therapeutic strategies.This study not only replicates but also extends the existing findings on the role of Aβ(1-38) (amyloid beta 1-38) in Alzheimer's disease (AD) in humans in vivo. Higher baseline Aβ(1-38) levels were associated with a decreased risk of conversion to AD dementia in subjective cognitive decline (SCD) and mild cognitive impairment (MCI). Different linear-mixed regression models suggest an association between higher Aβ(1-38) baseline levels and slower Preclinical Alzheimer's Cognitive Composite (PACC) and Clinical Dementia Rating Sum of Boxes (CDR-SB) decline. Including Aβ(1-40) beyond Aβ(1-38) in the model confirmed a link between Aβ(1-38) and PACC decline, but showed no association of Aβ(1-38) on CDR-SB and Mini-Mental State Examination (MMSE) decline. The impact of short Aβ isoforms in AD progression might have been under-investigated These findings underscore the urgent need for additional research on the role of these shorter Aβ peptides in AD, as they may hold key insights for future therapeutic strategies.
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000277323 650_7 $$2Other$$aAD conversion risk
000277323 650_7 $$2Other$$aAlzheimer's disease
000277323 650_7 $$2Other$$aAβ(1‐38)
000277323 650_7 $$2Other$$acerebrospinal fluid
000277323 650_7 $$2Other$$acognitive decline
000277323 650_7 $$2Other$$aneurotoxicity
000277323 650_7 $$2Other$$aprotective factor
000277323 650_7 $$2Other$$ashorter Aβ peptides
000277323 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000277323 650_7 $$2NLM Chemicals$$aPeptide Fragments
000277323 650_7 $$2NLM Chemicals$$aamyloid beta-protein (1-38)
000277323 650_7 $$2NLM Chemicals$$aBiomarkers
000277323 650_2 $$2MeSH$$aHumans
000277323 650_2 $$2MeSH$$aAmyloid beta-Peptides: cerebrospinal fluid
000277323 650_2 $$2MeSH$$aAlzheimer Disease: cerebrospinal fluid
000277323 650_2 $$2MeSH$$aDisease Progression
000277323 650_2 $$2MeSH$$aMale
000277323 650_2 $$2MeSH$$aFemale
000277323 650_2 $$2MeSH$$aPeptide Fragments: cerebrospinal fluid
000277323 650_2 $$2MeSH$$aAged
000277323 650_2 $$2MeSH$$aCognitive Dysfunction: cerebrospinal fluid
000277323 650_2 $$2MeSH$$aLongitudinal Studies
000277323 650_2 $$2MeSH$$aMental Status and Dementia Tests
000277323 650_2 $$2MeSH$$aBiomarkers: cerebrospinal fluid
000277323 650_2 $$2MeSH$$aMiddle Aged
000277323 650_2 $$2MeSH$$aAged, 80 and over
000277323 650_2 $$2MeSH$$aNeuropsychological Tests: statistics & numerical data
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000277323 7001_ $$0P:(DE-HGF)0$$avan Breukelen, Gerard$$b2
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000277323 7001_ $$0P:(DE-2719)2000055$$aLaske, Christoph$$b14$$udzne
000277323 7001_ $$0P:(DE-2719)9001516$$aMunk, Matthias H$$b15$$udzne
000277323 7001_ $$0P:(DE-2719)2812234$$aPerneczky, Robert$$b16$$udzne
000277323 7001_ $$0P:(DE-2719)9001808$$aRauchmann, Boris Stephan$$b17$$udzne
000277323 7001_ $$0P:(DE-2719)2811351$$aBuerger, Katharina$$b18$$udzne
000277323 7001_ $$0P:(DE-2719)9002557$$aJanowitz, Daniel$$b19$$udzne
000277323 7001_ $$0P:(DE-2719)2000005$$aDüzel, Emrah$$b20$$udzne
000277323 7001_ $$0P:(DE-2719)2811614$$aGlanz, Wenzel$$b21$$udzne
000277323 7001_ $$0P:(DE-2719)2000032$$aJessen, Frank$$b22$$udzne
000277323 7001_ $$0P:(DE-HGF)0$$aRostamzadeh, Ayda$$b23
000277323 7001_ $$0P:(DE-2719)2811317$$aWiltfang, Jens$$b24$$udzne
000277323 7001_ $$0P:(DE-2719)9000444$$aBartels, Claudia$$b25
000277323 7001_ $$0P:(DE-2719)2810394$$aKilimann, Ingo$$b26$$udzne
000277323 7001_ $$0P:(DE-2719)2812035$$aSchneider, Anja$$b27$$udzne
000277323 7001_ $$0P:(DE-2719)2811326$$aFliessbach, Klaus$$b28$$udzne
000277323 7001_ $$0P:(DE-2719)2811122$$aPriller, Josef$$b29$$udzne
000277323 7001_ $$0P:(DE-2719)2812446$$aSpruth, Eike Jakob$$b30
000277323 7001_ $$0P:(DE-2719)9003016$$aHellmann-Regen, Julian$$b31$$udzne
000277323 7001_ $$0P:(DE-2719)2811024$$aPeters, Oliver$$b32$$eLast author$$udzne
000277323 773__ $$0PERI:(DE-600)2201940-6$$a10.1002/alz.14545$$gVol. 21, no. 2, p. e14545$$n2$$pe14545$$tAlzheimer's and dementia$$v21$$x1552-5260$$y2025
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