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000281839 1001_ $$0P:(DE-2719)9002868$$aNeubauer, Antonia$$b0$$eFirst author$$udzne
000281839 245__ $$aAlpha-synuclein deposition patterns in Alzheimer's disease: association with cortical amyloid beta and variable tau load.
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000281839 520__ $$aAlpha-synuclein (α-syn) deposits are common in around half of the Alzheimer's disease (AD) cases. While direct and indirect protein interactions are suggested, the relationships between different protein aggregates remain poorly understood. Here, we aimed to characterize α-syn, amyloid beta (Aβ), and tau load distributions of AD patients. Protein deposits were automatically quantified with random forest pixel classifiers in immunohistochemical stains of up to 28 brain regions in 72 brains with advanced AD neuropathological change. α-syn-negative cases were distinguished from amygdala predominant, brainstem predominant, and cortical α-syn-positive cases. Relationships with age, sex, and ApoE genotype were examined. α-syn co-pathology was detected in 60% of AD cases, more frequently, although not significantly, in women. Half of these positive cases presented α-syn deposits in the cortex, around one-third predominantly in the amygdala, and the remaining cases primarily in the brainstem. A high α-syn load in the amygdala was associated with an increased cortical Aβ load. The cortical tau load was increased in the amygdala-predominant α-syn group, but decreased in the brainstem-predominant and cortical α-syn cases in comparison with α-syn-negative cases. ApoE4 was associated with higher hippocampal α-syn and cortical Aβ deposition. Younger age at death was associated with a focally higher Aβ and tau load. AD cases with cortical α-syn deposition tended to have a younger age at death. Here, we show that next to age, sex, and ApoE genotype, the α-syn distribution in AD is related to different Aβ and tau loads. This may have therapeutic relevance for identifying patients who respond to Aβ immunotherapy related to tau burden and underpin the need to define α-syn pathology and distribution in early disease stages.
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000281839 650_7 $$2Other$$aAlpha-synuclein
000281839 650_7 $$2Other$$aAlzheimer’s disease
000281839 650_7 $$2Other$$aImmunohistochemistry
000281839 650_7 $$2Other$$aLewy body disease
000281839 650_7 $$2Other$$aMixed pathology
000281839 650_7 $$2Other$$aQuantitative neuropathology
000281839 650_7 $$2NLM Chemicals$$aalpha-Synuclein
000281839 650_7 $$2NLM Chemicals$$atau Proteins
000281839 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000281839 650_7 $$2NLM Chemicals$$aApolipoproteins E
000281839 650_7 $$2NLM Chemicals$$aMAPT protein, human
000281839 650_2 $$2MeSH$$aHumans
000281839 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000281839 650_2 $$2MeSH$$aAlzheimer Disease: metabolism
000281839 650_2 $$2MeSH$$aAlzheimer Disease: genetics
000281839 650_2 $$2MeSH$$aFemale
000281839 650_2 $$2MeSH$$aMale
000281839 650_2 $$2MeSH$$aalpha-Synuclein: metabolism
000281839 650_2 $$2MeSH$$atau Proteins: metabolism
000281839 650_2 $$2MeSH$$aAmyloid beta-Peptides: metabolism
000281839 650_2 $$2MeSH$$aAged
000281839 650_2 $$2MeSH$$aAged, 80 and over
000281839 650_2 $$2MeSH$$aCerebral Cortex: metabolism
000281839 650_2 $$2MeSH$$aCerebral Cortex: pathology
000281839 650_2 $$2MeSH$$aMiddle Aged
000281839 650_2 $$2MeSH$$aBrain: pathology
000281839 650_2 $$2MeSH$$aBrain: metabolism
000281839 650_2 $$2MeSH$$aApolipoproteins E: genetics
000281839 7001_ $$0P:(DE-2719)9002869$$aWeissenbrunner, Doris$$b1$$udzne
000281839 7001_ $$0P:(DE-2719)9003673$$aPekrun, Susanna$$b2$$udzne
000281839 7001_ $$0P:(DE-HGF)0$$aRoeber, Sigrun$$b3
000281839 7001_ $$0P:(DE-HGF)0$$aRuf, Viktoria$$b4
000281839 7001_ $$0P:(DE-2719)9001363$$aFeyen, Paul$$b5$$udzne
000281839 7001_ $$0P:(DE-2719)2813904$$aStrübing, Felix L$$b6$$udzne
000281839 7001_ $$0P:(DE-2719)2810441$$aHerms, Jochen$$b7$$eLast author$$udzne
000281839 773__ $$0PERI:(DE-600)1458410-4$$a10.1007/s00401-025-02952-w$$gVol. 150, no. 1, p. 46$$n1$$p46$$tActa neuropathologica$$v150$$x0001-6322$$y2025
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