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<p>Alzheimer’s disease (AD), the most prevalent form of dementia worldwide has been recently conceptualised as Type 3 Diabetes (T3DM) due to mounting evidence linking brain insulin resistance and impaired glucose metabolism to neurodegeneration. The aim of this review is to unveil the molecular mechanism that shares the common pathologies of AD and Type 2 Diabetes (T2DM). The key evidence that links AD and T2DM that emphasizes the metabolic abnormalities which includes alteration in insulin signalling, neuroinflammation, oxidative stress, mitochondrial dysfunction. Recent research on neuroimaging studies revealed that the impaired glucose metabolism in AD vulnerable regions while molecular analysis show decreased insulin receptor expression and impaired insulin signalling pathways. Furthermore, shared molecular mechanism including oxidative stress, inflammation, protein misfolding, and mitochondrial dysfunction links metabolic and neurodegenerative processes. The conceptualization of AD as T3DM is supported by mechanistic evidence suggests by the brain insulin resistance. The understanding of metabolic perspective of AD opens up the possibility of employing novel therapeutic strategies that incorporate lifestyle modifications and the use of antidiabetic medications to mitigate cognitive decline.</p><p></p>

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Revisiting the Concept of Alzheimer’s Disease as Type 3 Diabetes Mellitus- A Critical Examination of Neuro-metabolic Link

  • 期刊论文

  • 发表日期：

    2026年4月30日

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  • M. Sathya,
  • P. Sangeetha,
  • V. Senthamarai Selvi,
  • K. Rekha

摘要

Alzheimer’s disease (AD), the most prevalent form of dementia worldwide has been recently conceptualised as Type 3 Diabetes (T3DM) due to mounting evidence linking brain insulin resistance and impaired glucose metabolism to neurodegeneration. The aim of this review is to unveil the molecular mechanism that shares the common pathologies of AD and Type 2 Diabetes (T2DM). The key evidence that links AD and T2DM that emphasizes the metabolic abnormalities which includes alteration in insulin signalling, neuroinflammation, oxidative stress, mitochondrial dysfunction. Recent research on neuroimaging studies revealed that the impaired glucose metabolism in AD vulnerable regions while molecular analysis show decreased insulin receptor expression and impaired insulin signalling pathways. Furthermore, shared molecular mechanism including oxidative stress, inflammation, protein misfolding, and mitochondrial dysfunction links metabolic and neurodegenerative processes. The conceptualization of AD as T3DM is supported by mechanistic evidence suggests by the brain insulin resistance. The understanding of metabolic perspective of AD opens up the possibility of employing novel therapeutic strategies that incorporate lifestyle modifications and the use of antidiabetic medications to mitigate cognitive decline.