Brain insulin resistance in type 2 diabetes and Alzheimer disease: concepts and conundrums
Open accessAbstract
Considerable overlap has been identified in the risk factors, comorbidities and putative pathophysiological mechanisms of Alzheimer disease and related dementias (ADRDs) and type 2 diabetes mellitus (T2DM), two of the most pressing epidemics of our time. Much is known about the biology of each condition, but whether T2DM and ADRDs are parallel phenomena arising from coincidental roots in ageing or synergistic diseases linked by vicious pathophysiological cycles remains unclear. Insulin resistance is a core feature of T2DM and is emerging as a potentially important feature of ADRDs. Here, we review key observations and experimental data on insulin signalling in the brain, highlighting its actions in neurons and glia. In addition, we define the concept of 'brain insulin resistance' and review the growing, although still inconsistent, literature concerning cognitive impairment and neuropathological abnormalities in T2DM, obesity and insulin resistance. Lastly, we review evidence of intrinsic brain insulin resistance in ADRDs. By expanding our understanding of the overlapping mechanisms of these conditions, we hope to accelerate the rational development of preventive, disease-modifying and symptomatic treatments for cognitive dysfunction in T2DM and ADRDs alike.
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Glucose metabolism is markedly reduced in Alzheimer disease and amnestic mild cognitive impairment.
“in AD and amnestic mild cognitive impairment (aMCI) glucose metabolism is dramatically decreased”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [7]
The section “Brain insulin resistance in ADRD, irrespective of T2DM” (page unavailable) describes glucose hypometabolism observed in Alzheimer disease. It also discusses MCI and reports improved FDG-PET metabolism after insulin treatment in a group with AD or MCI, but does not establish that glucose metabolism is markedly reduced specifically in amnestic MCI. (LLM, conf=0.84)
Experimental — accuracy not yet measuredBrain insulin resistance occurs in Alzheimer disease and amnestic mild cognitive impairment.
“In AD and aMCI, however, brain insulin resistance is present6,7.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [7]
The section “Brain insulin resistance in ADRD, irrespective of T2DM” reports experimentally demonstrated brain insulin resistance in AD and insulin-signalling abnormalities in post-mortem brains from people with AD or MCI. It does not specify that the MCI cases were amnestic, so the aMCI-specific part of the claim is not established by our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredGlucose enters the brain through efficient transporters and needs insulin for optimal cellular use.
“Glucose enters the brain from the vasculature through highly efficient glucose transporters and requires insulin for optimal cellular utilization7.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [7]
The “Effects of insulin in neurons” section describes glucose uptake through GLUT3 and says insulin-regulated GLUT4 may improve glucose flux during high metabolic demand. It also explicitly says neuronal glucose uptake and utilization are influenced by insulin, not dependent on it. The source therefore does not support the general claim that optimal cellular use requires insulin. (LLM, conf=0.87)
Experimental — accuracy not yet measuredGlucose metabolism is significantly impaired in Alzheimer disease and amnestic mild cognitive impairment brains.
“Yet glucose metabolism in AD and aMCI brains is significantly impaired5–7,9,38.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [7]
In “Brain insulin resistance in ADRD, irrespective of T2DM” (page unavailable), the review explicitly describes glucose hypometabolism in AD. It also reports abnormal insulin signalling in AD and MCI and improved FDG-PET metabolism after treatment in a combined AD/MCI group, but does not establish the claimed significant impairment of glucose metabolism specifically in amnestic MCI brains. (LLM, conf=0.83)
Experimental — accuracy not yet measuredThe brain has high energy demands and depends heavily on efficient ATP production through glycolysis, the TCA cycle, and oxidative phosphorylation.
“The brain is an energy-demanding organ and relies heavily on efficient ATP production via glycolysis, the TCA cycle and oxidative phosphorylation (Fig. 1)7.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [7]
The “Effects of insulin in neurons” section describes glucose as the brain’s major energy source and links glucose uptake to local energy demand. The “Effects of insulin in glial cells” section describes glycolytic processing of glucose and neuronal ATP production through oxidative phosphorylation during high energy demand. Our copy does not mention the TCA cycle or present all three pathways together as the basis of the brain’s ATP production; page numbers were not available. (LLM, conf=0.84)
Experimental — accuracy not yet measured
Besides mTOR activation, insulin resistance can cause neuronal glucose deficiency, leading to reduced glucose metabolism, impaired ATP production, and neuronal dysfunction or death.
“In addition to mTOR activation, insulin resistance can also result in neuronal glucose deficiency, with consequent decreased glucose metabolism, impaired ATP production, and dysfunction and/or death7,42”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [7]
The “Effects of insulin in neurons” section says insulin can influence neuronal glucose uptake through GLUT4 and promotes neuronal survival. It also says most neuronal glucose uptake occurs through insulin-independent GLUT3. The paper does not establish the claimed sequence from insulin resistance to neuronal glucose deficiency, impaired ATP production, and dysfunction or death. (LLM, conf=0.84)
Experimental — accuracy not yet measuredPossible action of Al in the pathogenesis of diabetes mellitus and concurrence of neurological disorders associated with Alzheimer's disease and other dementias point to a common cellular basis of the pathogenesis of both metabolic and cognitive disorders, which can arise from toxic actions of Al.
“The possible action of Al in the pathogenesis of diabetes mellitus and the concurrence of neurological disorders associated with Alzheimer’s disease and other dementias (Arnold et al., 2018) point to the common cellular basis of the pathogenesis of both metabolic and cognitive disorders, which can arise from toxic actions of Al.”
From Aluminium toxicosis: a review of toxic actions and effects (2019) · cites this paper as Arnold et al., 2018
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredInsulin resistance affects neuronal function and Aβ accumulation in the brain, contributing to neuroinflammation, synaptic dysfunction, and cognitive decline.
“insulin resistance could affect neuronal function and Aβ accumulation in the brain, which contribute to neuroinflammation and synaptic dysfunction and finally lead to cognitive decline (Arnold et al., 2018).”
From AD-Like Neuropsychiatric Dysfunction in a Mice Model Induced by a Combination of High-Fat Diet and Intraperitoneal Injection of Streptozotocin (2024) · cites this paper as Arnold et al., 2018
The ‘Effects of insulin in neurons’ section describes insulin’s roles in neuronal and synaptic function, and ‘Systemic insulin resistance and ADRDs’ reports animal-model evidence for amyloid-β accumulation. The review also reports associations between abnormal brain insulin signalling and poorer cognition in ‘Brain insulin resistance in ADRD, irrespective of T2DM.’ It does not establish the claimed sequence through neuroinflammation and synaptic dysfunction to cognitive decline; it notes that human evidence linking systemic insulin resistance to amyloid-β pathology is mostly negative. Page numbers were not available in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThere is a potential link between AD and insulin resistance, with decreased key insulin signaling proteins and increased insulin resistance markers in the brains of AD mice.
“Recent studies have suggested a potential link between AD and insulin resistance, which exhibits a decreased level of key insulin signaling proteins and an increased level of insulin resistance markers in the brains of AD mice (Craft et al., 1998; Arnold et al., 2018; Kshirsagar et al., 2021).”
From AD-Like Neuropsychiatric Dysfunction in a Mice Model Induced by a Combination of High-Fat Diet and Intraperitoneal Injection of Streptozotocin (2024) · cites this paper as Arnold et al., 2018
The section “Brain insulin resistance in ADRD, irrespective of T2DM” reports reduced insulin-signalling proteins and abnormal markers of insulin resistance in post-mortem brains of people with AD, supporting the proposed link. It does not establish the claimed decreases and increases in the brains of AD mice; the population in the cited passages is human. Page numbers were not available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredType 2 diabetes, in which insulin resistance is a key feature, is a significant risk factor for Alzheimer disease.
“Indeed, type 2 diabetes (T2DM), a key component of which is insulin resistance, is a significant risk factor for developing AD7.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [7]
mTOR-mediated events may help explain why type 2 diabetes is a significant risk factor for Alzheimer disease.
“These mTOR-mediated events may help explain the observation that type 2 diabetes (T2DM) is a significant risk factor for development of AD7,41.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [7]
Brain insulin resistance is common in Alzheimer disease.
“Brain insulin resistance is common in AD7,38,41.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [7]
Mitochondrial dysfunction and insulin resistance are closely related.
“Indeed, mitochondrial dysfunction and insulin resistance are intimately related7,38.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [7]
The ‘Systemic and brain insulin resistance’ section links systemic and brain insulin resistance, but does not discuss their relationship with mitochondrial dysfunction. A search for ‘mitochondrial’ found a study title in the References concerning mitochondrial abnormalities in mouse models; the paper’s text does not state the claimed relationship. (LLM, conf=0.72)
Experimental — accuracy not yet measuredBrain insulin resistance might involve down-regulation or failure of insulin receptors and impairments of downstream signalling, and contribute to the emergence and/or persistence of metabolic dysregulation.
“it might involve the down-regulation or failure of insulin receptors, as well as impairments of downstream signalling, and contribute to the emergence and/or persistence of metabolic dysregulation”
From Intranasal insulin (2021) · cites this paper as [90]
Insulin may boost brain energy supply via effects on astrocytes and other glia cells, including oligodendrocytes.
“Insulin may moreover boost brain energy supply via effects on astrocytes 129 and other glia cells, including oligodentrocytes.90”
From Intranasal insulin (2021) · cites this paper as [90]
Respective organ deficits in type 2 diabetes include reductions in hippocampal volume, ischaemic impairments and cortical hypometabolism.
“Respective organ deficits include reductions in hippocampal volume, 141 as well as ischaemic impairments and cortical hypometabolism.90”
From Intranasal insulin (2021) · cites this paper as [90]
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- Authors
- Arnold, S. E., Arvanitakis, Z., Macauley-Rambach, S. L., Koenig, A. M., Wang, H.-Y., Ahima, R. S., Craft, S., Gandy, S., Buettner, C., Stoeckel, L. E., Holtzman, D. M., & Nathan, D. M.
- Affiliations
- Harvard University (US)
- Rush University Medical Center (US)
- City University of New York (US)
- Johns Hopkins University (US)
- Atrium Health Wake Forest Baptist (US)
- Icahn School of Medicine at Mount Sinai (US)
- Washington University in St. Louis (US)
- Corresponding author
- Arnold, Steven E.
- ORCID
- Venue
- Nature Reviews Neurology
- Published
- 2018-01-29
- Volume
- 14
- Issue
- 3
- Pages
- 168-181
- ISSN
- 1759-4758 (ISSN-L)
- 1759-4766
- PMC
- PMC6098968
- OpenAlex
- W2786962139
- Cited by
- 1,597
- References
- 286
- Citations by year
- 2026: 223 · 2025: 244 · 2024: 218 · 2023: 205 · 2022: 210 · 2021: 176 · 2020: 163 · 2019: 102 · 2018: 52 · 2015: 1 · 2012: 1
- FWCI
- 16.18
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Neurology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Rutgers University Community Repository (Rutgers University) (submittedVersion)
- Funders
- BrightFocus Foundation
- National Institutes of Health
- National Institute on Aging (R21AG051958)
- National Institute of Neurological Disorders and Stroke (R01NS084965)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- brain insulin resistance, type 2 diabetes, Alzheimer's disease, Alzheimer's disease and related dementias, insulin signaling, cognitive impairment, obesity, glia, neurons, neuropathology, comorbidities, aging
- MeSH terms
- Brain, Dementia, Diabetes Mellitus, Type 2, Humans, Insulin, Insulin Resistance
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