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@ARTICLE{Ayoub:281646,
      author       = {Ayoub, Sama and Arabi, Maryam and Al-Najjar, Yousef and
                      Laswi, Ibrahim and Outeiro, Tiago F and Chaari, Ali},
      title        = {{G}lycation in {A}lzheimer's {D}isease and {T}ype 2
                      {D}iabetes: {T}he {P}rospect of {D}ual {D}rug {A}pproaches
                      for {T}herapeutic {I}nterventions.},
      journal      = {Molecular neurobiology},
      volume       = {62},
      number       = {11},
      issn         = {0893-7648},
      address      = {Totowa, NJ},
      publisher    = {Humana Press},
      reportid     = {DZNE-2025-01164},
      pages        = {14859 - 14882},
      year         = {2025},
      abstract     = {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.},
      subtyp        = {Review Article},
      keywords     = {Alzheimer Disease: drug therapy / Alzheimer Disease:
                      metabolism / Humans / Diabetes Mellitus, Type 2: drug
                      therapy / Diabetes Mellitus, Type 2: metabolism / Glycation
                      End Products, Advanced: metabolism / Animals / Hypoglycemic
                      Agents: therapeutic use / Hypoglycemic Agents: pharmacology
                      / Gastrointestinal Microbiome: drug effects / Advanced
                      glycation end products (AGEs) (Other) / Alzheimer’s
                      disease (Other) / Dual drugs (Other) / Type 2 diabetes
                      (Other) / Glycation End Products, Advanced (NLM Chemicals) /
                      Hypoglycemic Agents (NLM Chemicals)},
      cin          = {AG Fischer},
      ddc          = {570},
      cid          = {I:(DE-2719)1410002},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40402411},
      doi          = {10.1007/s12035-025-05051-9},
      url          = {https://pub.dzne.de/record/281646},
}