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000282327 037__ $$aDZNE-2025-01288
000282327 041__ $$aEnglish
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000282327 1001_ $$0P:(DE-2719)9000358$$aZafar, Saima$$b0$$udzne
000282327 245__ $$aProteomic Profiling Reveals Mitochondrial Dysregulation in Rapidly Progressive Alzheimer's: Role of DLDH in Amyloid Beta Aggregation.
000282327 260__ $$aTotowa, NJ$$bHumana Press$$c2025
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000282327 520__ $$aAlzheimer's disease (AD) is presented as multiple clinical variants depending upon the rate of progression and familial background; however, the exact molecular mechanisms associated with these subtypes and their treatments are yet to be understood. The current study is based on a global proteome analysis of brain samples from patients (n = 38) with rapidly progressive AD (rpAD-survival time < 3 years), sporadic AD (spAD-survival time of 8-10 years), and healthy controls. Proteome analysis revealed a differential regulation of 79 proteins and highlighted the dysregulation of mitochondrial machinery and glucose metabolism in rpAD. Dihydrolipoamide dehydrogenase (DLDH), a mitochondrial oxidoreductase, showed a significant reduction and delocalization in rpAD. In vitro analysis revealed a potential role of DLDH in the aggregation of amyloid beta. Rapid progression in AD may be influenced by the energy homeostasis and redox dysfunction linked with the DLDH.
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000282327 650_7 $$2Other$$aAlzheimer’s disease (AD)
000282327 650_7 $$2Other$$aDLDH
000282327 650_7 $$2Other$$aMetabolic networks
000282327 650_7 $$2Other$$aMetabolism
000282327 650_7 $$2Other$$aPost-translational modification
000282327 650_7 $$2Other$$aProteomics
000282327 650_7 $$2Other$$aRapidly progressive Alzheimer’s disease (rpAD)
000282327 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000282327 650_7 $$2NLM Chemicals$$aProtein Aggregates
000282327 650_2 $$2MeSH$$aHumans
000282327 650_2 $$2MeSH$$aAlzheimer Disease: metabolism
000282327 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000282327 650_2 $$2MeSH$$aAmyloid beta-Peptides: metabolism
000282327 650_2 $$2MeSH$$aProteomics: methods
000282327 650_2 $$2MeSH$$aMitochondria: metabolism
000282327 650_2 $$2MeSH$$aMitochondria: pathology
000282327 650_2 $$2MeSH$$aMale
000282327 650_2 $$2MeSH$$aFemale
000282327 650_2 $$2MeSH$$aDisease Progression
000282327 650_2 $$2MeSH$$aAged
000282327 650_2 $$2MeSH$$aProtein Aggregation, Pathological: metabolism
000282327 650_2 $$2MeSH$$aBrain: metabolism
000282327 650_2 $$2MeSH$$aBrain: pathology
000282327 650_2 $$2MeSH$$aProtein Aggregates
000282327 650_2 $$2MeSH$$aAged, 80 and over
000282327 7001_ $$aNoor, Aneeqa$$b1
000282327 7001_ $$0P:(DE-2719)9001558$$aYounas, Neelam$$b2$$udzne
000282327 7001_ $$0P:(DE-2719)9000295$$aShafiq, Mohsin$$b3
000282327 7001_ $$0P:(DE-2719)2811355$$aDittmar, Kathrin$$b4
000282327 7001_ $$aYagensky, Oleksandr$$b5
000282327 7001_ $$0P:(DE-2719)9000287$$aSchmitz, Matthias$$b6$$udzne
000282327 7001_ $$aFerrer, Isidre$$b7
000282327 7001_ $$0P:(DE-2719)2812183$$aHermann, Peter$$b8
000282327 7001_ $$0P:(DE-2719)2000058$$aZerr, Inga$$b9$$eLast author$$udzne
000282327 773__ $$0PERI:(DE-600)2079384-4$$a10.1007/s12035-025-05327-0$$gVol. 63, no. 1, p. 73$$n1$$p73$$tMolecular neurobiology$$v63$$x0893-7648$$y2025
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