Home > Documents in Process > Proteomic Profiling Reveals Mitochondrial Dysregulation in Rapidly Progressive Alzheimer's: Role of DLDH in Amyloid Beta Aggregation. > print

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024 7 _ |a 10.1007/s12035-025-05327-0
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037 _ _ |a DZNE-2025-01288
041 _ _ |a English
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100 1 _ |a Zafar, Saima
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245 _ _ |a Proteomic Profiling Reveals Mitochondrial Dysregulation in Rapidly Progressive Alzheimer's: Role of DLDH in Amyloid Beta Aggregation.
260 _ _ |a Totowa, NJ
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|b Humana Press
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520 _ _ |a Alzheimer'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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650 _ 7 |a Alzheimer’s disease (AD)
|2 Other
650 _ 7 |a DLDH
|2 Other
650 _ 7 |a Metabolic networks
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650 _ 7 |a Metabolism
|2 Other
650 _ 7 |a Post-translational modification
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650 _ 7 |a Proteomics
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650 _ 7 |a Rapidly progressive Alzheimer’s disease (rpAD)
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650 _ 7 |a Amyloid beta-Peptides
|2 NLM Chemicals
650 _ 7 |a Protein Aggregates
|2 NLM Chemicals
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Alzheimer Disease: metabolism
|2 MeSH
650 _ 2 |a Alzheimer Disease: pathology
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: metabolism
|2 MeSH
650 _ 2 |a Proteomics: methods
|2 MeSH
650 _ 2 |a Mitochondria: metabolism
|2 MeSH
650 _ 2 |a Mitochondria: pathology
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Disease Progression
|2 MeSH
650 _ 2 |a Aged
|2 MeSH
650 _ 2 |a Protein Aggregation, Pathological: metabolism
|2 MeSH
650 _ 2 |a Brain: metabolism
|2 MeSH
650 _ 2 |a Brain: pathology
|2 MeSH
650 _ 2 |a Protein Aggregates
|2 MeSH
650 _ 2 |a Aged, 80 and over
|2 MeSH
700 1 _ |a Noor, Aneeqa
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700 1 _ |a Younas, Neelam
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700 1 _ |a Shafiq, Mohsin
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700 1 _ |a Dittmar, Kathrin
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700 1 _ |a Yagensky, Oleksandr
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700 1 _ |a Schmitz, Matthias
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700 1 _ |a Ferrer, Isidre
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700 1 _ |a Hermann, Peter
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700 1 _ |a Zerr, Inga
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773 _ _ |a 10.1007/s12035-025-05327-0
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|t Molecular neurobiology
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