Home > Documents in Process > Glycation in Alzheimer's Disease and Type 2 Diabetes: The Prospect of Dual Drug Approaches for Therapeutic Interventions. > print

001     281646
005     20251010152028.0
024 7 _ |a 10.1007/s12035-025-05051-9
|2 doi
024 7 _ |a pmid:40402411
|2 pmid
024 7 _ |a 0893-7648
|2 ISSN
024 7 _ |a 1559-1182
|2 ISSN
037 _ _ |a DZNE-2025-01164
041 _ _ |a English
082 _ _ |a 570
100 1 _ |a Ayoub, Sama
|b 0
245 _ _ |a Glycation in Alzheimer's Disease and Type 2 Diabetes: The Prospect of Dual Drug Approaches for Therapeutic Interventions.
260 _ _ |a Totowa, NJ
|c 2025
|b Humana Press
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1760102342_23892
|2 PUB:(DE-HGF)
|x Review Article
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a As global life expectancy increases, the prevalence of neurodegenerative diseases like Alzheimer's disease (AD) continues to rise. Since therapeutic options are minimal, a deeper understanding of the pathophysiology is essential for improved diagnosis and treatments. AD is marked by the aggregation of Aβ proteins, tau hyperphosphorylation, and progressive neuronal loss, though its precise origins remain poorly understood. Meanwhile, type 2 diabetes mellitus (T2DM) is characterized by chronic hyperglycemia, leading to the formation of advanced glycation end products (AGEs), which are implicated in tissue damage and neurotoxicity. These AGEs can be resistant to proteolysis and, therefore, accumulate, exacerbating AD pathology and accelerating neurodegeneration. Insulin resistance, a hallmark of T2DM, further complicates AD pathogenesis by promoting tau hyperphosphorylation and Aβ plaque accumulation. Additionally, gut microbiome dysbiosis in T2DM fosters AGE accumulation and neuroinflammation, underscoring the intricate relationship between metabolic disorders, gut health, and neurodegenerative processes. This complex interplay presents both a challenge and a potential avenue for therapeutic intervention. Emerging evidence suggests that antidiabetic medications may offer cognitive benefits in AD, as well as in other neurodegenerative conditions, pointing to a shared pathophysiology. Thus, we posit that targeting AGEs, insulin signaling, and gut microbiota dynamics presents promising opportunities for innovative treatment approaches in AD and T2DM.
536 _ _ |a 352 - Disease Mechanisms (POF4-352)
|0 G:(DE-HGF)POF4-352
|c POF4-352
|f POF IV
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
650 _ 7 |a Advanced glycation end products (AGEs)
|2 Other
650 _ 7 |a Alzheimer’s disease
|2 Other
650 _ 7 |a Dual drugs
|2 Other
650 _ 7 |a Type 2 diabetes
|2 Other
650 _ 7 |a Glycation End Products, Advanced
|2 NLM Chemicals
650 _ 7 |a Hypoglycemic Agents
|2 NLM Chemicals
650 _ 2 |a Alzheimer Disease: drug therapy
|2 MeSH
650 _ 2 |a Alzheimer Disease: metabolism
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Diabetes Mellitus, Type 2: drug therapy
|2 MeSH
650 _ 2 |a Diabetes Mellitus, Type 2: metabolism
|2 MeSH
650 _ 2 |a Glycation End Products, Advanced: metabolism
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Hypoglycemic Agents: therapeutic use
|2 MeSH
650 _ 2 |a Hypoglycemic Agents: pharmacology
|2 MeSH
650 _ 2 |a Gastrointestinal Microbiome: drug effects
|2 MeSH
700 1 _ |a Arabi, Maryam
|b 1
700 1 _ |a Al-Najjar, Yousef
|b 2
700 1 _ |a Laswi, Ibrahim
|b 3
700 1 _ |a Outeiro, Tiago F
|0 P:(DE-2719)2814138
|b 4
|u dzne
700 1 _ |a Chaari, Ali
|b 5
773 _ _ |a 10.1007/s12035-025-05051-9
|g Vol. 62, no. 11, p. 14859 - 14882
|0 PERI:(DE-600)2079384-4
|n 11
|p 14859 - 14882
|t Molecular neurobiology
|v 62
|y 2025
|x 0893-7648
856 4 _ |u https://pub.dzne.de/record/281646/files/DZNE-2025-01164.pdf
|y Restricted
856 4 _ |u https://pub.dzne.de/record/281646/files/DZNE-2025-01164.pdf?subformat=pdfa
|x pdfa
|y Restricted
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 4
|6 P:(DE-2719)2814138
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-352
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Disease Mechanisms
|x 0
915 _ _ |a DEAL Springer
|0 StatID:(DE-HGF)3002
|2 StatID
|d 2025-01-07
|w ger
915 _ _ |a DEAL Springer
|0 StatID:(DE-HGF)3002
|2 StatID
|d 2025-01-07
|w ger
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2025-01-07
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|d 2025-01-07
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2025-01-07
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
|d 2025-01-07
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0160
|2 StatID
|b Essential Science Indicators
|d 2025-01-07
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1190
|2 StatID
|b Biological Abstracts
|d 2025-01-07
915 _ _ |a WoS
|0 StatID:(DE-HGF)0113
|2 StatID
|b Science Citation Index Expanded
|d 2025-01-07
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
|d 2025-01-07
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b MOL NEUROBIOL : 2022
|d 2025-01-07
915 _ _ |a IF >= 5
|0 StatID:(DE-HGF)9905
|2 StatID
|b MOL NEUROBIOL : 2022
|d 2025-01-07
920 1 _ |0 I:(DE-2719)1410002
|k AG Fischer
|l Epigenetics and Systems Medicine in Neurodegenerative Diseases
|x 0
980 _ _ |a journal
980 _ _ |a EDITORS
980 _ _ |a VDBINPRINT
980 _ _ |a I:(DE-2719)1410002
980 _ _ |a UNRESTRICTED

LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21