ReviewMetabolic brain disease2015
Role of insulin resistance in Alzheimer's disease.
Review in Metabolic brain disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- Glucose-Lowering Therapies and Cognitive Decline: From Molecular Mechanisms to Clinical Evidence and Future Perspectives.Advances in therapy · 2026Review
- Protein glycoxidation in neuropsychiatric disorders-from basic research to clinical practice.Redox biology · 2026Review
- The metabolic roots of memory loss: interlinking the Diabetes-Alzheimer's hypothesis.Metabolic brain disease · 2026Review
- Potential Applications of Natural Components of Traditional Chinese Medicine Delivery via Nanoparticle Drug Delivery Systems in the Treatment of Alzheimer's Disease.International journal of nanomedicine · 2025Review
- Potential molecular mechanism of exercise reversing insulin resistance and improving neurodegenerative diseases.Frontiers in physiology · 2024Review
- Hot Spots for the Use of Intranasal Insulin: Cerebral Ischemia, Brain Injury, Diabetes Mellitus, Endocrine Disorders and Postoperative Delirium.International journal of molecular sciences · 2023Review
- Intermittent theta burst stimulation attenuates oxidative stress and reactive astrogliosis in the streptozotocin-induced model of Alzheimer's disease-like pathology.Frontiers in aging neuroscience · 2023Article
- Hyperinsulinemia-induced microglial mitochondrial dynamic and metabolic alterations lead to neuroinflammationFrontiers in neuroscience · 2022Article
- Based on molecular structures: Amyloid-β generation, clearance, toxicity and therapeutic strategies.Frontiers in molecular neuroscience · 2022Review
- Diabetes and Alzheimer's Disease: Might Mitochondrial Dysfunction Help Deciphering the Common Path?Antioxidants (Basel, Switzerland) · 2021Review
- Oral administration of Centella asiatica (L.) Urb leave aqueous extract ameliorates cerebral oxidative stress, inflammation, and apoptosis in male rats with type-2 diabetes.Inflammopharmacology · 2020Article
- Iron Deposition Leads to Hyperphosphorylation of Tau and Disruption of Insulin Signaling.Frontiers in neurology · 2019Article
- Birth weight and catch up growth are associated with childhood impulsivity in two independent cohorts.Scientific reports · 2018Article
- Suppressor of Cytokine Signaling 3: Emerging Role Linking Central Insulin Resistance and Alzheimer's Disease.Frontiers in neuroscience · 2018Review
- The association between PGC-1α and Alzheimer's disease.Anatomy & cell biology · 2016Review
- Role of berberine in Alzheimer's disease.Neuropsychiatric disease and treatment · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A critical role of insulin resistance (IR) in Alzheimer's disease (AD) includes beta-amyloid (Aβ) production and accumulation, the formation of neurofibrillary tangles (NFTs), failure of synaptic transmission and neuronal degeneration. Aβ is sequentially cleavaged from APP by two proteolytic enzymes: β-secretase and γ-secretase. IR could regulate Aβ production via enhancing β- and γ-secretase activity. Meanwhile, IR induces oxidative stress and inflammation in the brain which contributes to Aβ and tau pathology. Aβ accumulation can enhance IR through Aβ-mediated inflammation and oxidative stress. IR is a possible linking between amyloid plaques and NFTs pathology via oxidative stress and neuroinflammation. Additionally, IR could disrupt acetylcholine activity, and accelerate axon degeneration and failures in axonal transport, and lead to cognitive impairment in AD. Preclinical and clinical studies have supported that insulin could be useful in the treatment of AD. Thus, an effective measure to inhibit IR may be a novel drug target in AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.