Cited by 621Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Is Alzheimer’s disease a type 3 diabetes? A critical appraisal

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Kandimalla, Ramesh, Thirumala, Vani, Reddy, P. Hemachandra·2017·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Abstract

Recently researchers proposed the term ‘Type-3-Diabetes’ for Alzheimer’s disease (AD) because of the shared molecular and cellular features among Type-1-Diabetes, Type-2-Diabetes and insulin resistance associated with memory deficits and cognitive decline in elderly individuals. Recent clinical and basic studies on patients with diabetes and AD revealed previously unreported cellular and pathological among diabetes, insulin resistance and AD. These studies are also strengthened by various basic biological studies that decipher the effects of insulin in the pathology of AD through cellular and molecular mechanisms. For instance, insulin is involved in the activation of glycogen synthase kinase 3β, which in turn causes phosphorylation of tau, which involved in the formation of neurofibrillary tangles. Interestingly, insulin also plays a crucial role in the formation amyloid plaques. In this review, we discussed significant shared mechanisms between AD and diabetes and we also provided therapeutic avenues for diabetes and AD.

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Crossref · 10.1016/j.bbadis.2016.08.018

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  • Alzheimer's disease shares multiple mechanisms with type 1 and type 2 diabetes mellitus, leading to the term 'type 3 diabetes'.

    “researchers have used the term “type 3 diabetes”, first proposed over a decade ago, [74] to refer to Alzheimer’s disease due to the plethora of shared mechanisms implicated both in AD and type 1 and type 2 diabetes mellitus (T1DM and T2DM) [75].”
  • Increased oxidative stress and mitochondrial dysfunction in critical brain areas cause neurodegeneration implicated in AD and PD, and these occur due to insulin resistance in T2DM.

    “Increased oxidative stress and mitochondrial dysfunction, which are mentioned above and occur in critical brain areas to cause neurodegeneration implicated in diseases, such as AD and PD [73], occur due to insulin resistance in T2DM [75].”
  • Brain insulin resistance is involved in cellular and molecular mechanisms of neurofibrillary tangles formation and amyloid plaques.

    “Indeed, brain insulin resistance has been shown to be involved in cellular and molecular mechanisms of neurofibrillary tangles formation and amyloid plaques [110], leading to AD being referred to as type III diabetes.”
  • Recent studies have regarded Alzheimer's disease as type 3 diabetes because of insulin signaling pathways damage.

    “Recent studies have regarded Alzheimer's disease as type 3 diabetes because of insulin signaling pathways damage (123).”

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Research works printed but not linked: 6

  1. [16]Cole AR Astell A Green C Sutherland C Molecular connexions between dementia and diabetes Neurosci Biobehav Rev 2007 31 1046 1063 17544131
  2. [69]Lin JW Ju W Foster K Lee SH Ahmadian G Wyszynski M Wang YT Sheng M Distinct molecular mechanisms and divergent endocytotic pathways of AMPA receptor internalization Nat Neurosci 2000 3 1282 1290 11100149
  3. [86]Hotamisligil GS Inflammatory pathways and insulin action Int J Obes Relat Metab Disord 2003 27 Suppl 3 S53 S55 14704746
  4. [132]Benedict C Hallschmid M Hatke A Schultes B Fehm HL Born J Kern W Intranasal insulin improves memory in humans Psychoneuroendocrinology 2004 29 1326 1334 15288712
  5. [147]Luchsinger JA Tang MX Shea S Mayeux R Hyperinsulinemia and risk of Alzheimer disease Neurology 2004 63 1187 1192 15477536
  6. [181]Gasparini L Gouras GK Wang R Gross RS Beal MF Greengard P Xu H Stimulation of beta-amyloid precursor protein trafficking by insulin reduces intraneuronal beta-amyloid and requires mitogen-activated protein kinase signaling J Neurosci 2001 21 2561 2570 11306609 PMC6762523

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Authors
Kandimalla, R., Thirumala, V., & Reddy, P. H.
Affiliations
  • Texas Tech University (US)
  • The University of Texas at Austin (US)
Corresponding author
Kandimalla, Ramesh
Venue
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Publisher
Elsevier BV
Published
2017-05
Volume
1863
Issue
5
Pages
1078-1089
ISSN
0925-4439 (ISSN-L)
OpenAlex
W2515127987
Cited by
621
References
189
Citations by year
2026: 33 · 2025: 72 · 2024: 82 · 2023: 77 · 2022: 75 · 2021: 81 · 2020: 75 · 2019: 56 · 2018: 35 · 2017: 32 · 2016: 3
FWCI
4.88
Type
journal article
Language
en
Open access
Locations
  • Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • NIH (AG042178, AG047812)
  • Garrison Family Foundation
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, type 3 diabetes, insulin resistance, insulin signaling, glycogen synthase kinase-3β, tau phosphorylation, neurofibrillary tangles, amyloid plaques, cognitive decline, memory impairment
MeSH terms
Glycogen Synthase Kinase 3 beta, Alzheimer Disease, Amyloid, Animals, Diabetes Mellitus, Humans, Insulin, Phosphorylation, tau Proteins

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