ReviewPharmaceuticals (Basel, Switzerland)2018
The Implication of the Brain Insulin Receptor in Late Onset Alzheimer's Disease Dementia.
Review in Pharmaceuticals (Basel, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 60 citations in OpenAlex.
- Transcriptomic signatures of treatment response to the combination of escitalopram and memantine or placebo in late-life depression.Molecular psychiatry · 2021Trial
- Understanding the Intersection Between Hormonal Dynamics and Brain Plasticity in Alzheimer's Disease: A Narrative Review for Implementing New Therapeutic Strategies.Health science reports · 2025Review
- Limettin and PD98059 Mitigated Alzheimer's Disease Like Pathology Induced by Streptozotocin in Mouse Model: Role of p-ERK1/2/p-GSK-3β/p-CREB/BDNF Pathway.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
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- Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025Review
- Cytosolic phospholipase A2 links tau pathology to insulin signaling impairment in Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- New Insights into the Role of SGLT-2 Inhibitors in the Prevention of Dementia.Neurology international · 2024Review
- Mind the Metabolic Gap: Bridging Migraine and Alzheimer's disease through Brain Insulin Resistance.Aging and disease · 2024Review
- Nitrooxidative Stress and Neuroinflammation Caused by Air Pollutants Are Associated with the Biological Markers of Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- Multi-cohort cerebrospinal fluid proteomics identifies robust molecular signatures for asymptomatic and symptomatic Alzheimer's disease.Research square · 2024Article
- Cytokine enrichment in deep cerebellar nuclei is contributed by multiple glial populations and linked to reduced amyloid plaque pathology.Journal of neuroinflammation · 2023Article
- Review
- Article
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- The Expression of Insulin in the Central Nervous System: What Have We Learned So Far?International journal of molecular sciences · 2023Review
- Fragile X mental retardation protein coordinates neuron-to-glia communication for clearance of developmentally transient brain neurons.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Insulin and Insulin Resistance in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- A multitude of signaling pathways associated with Alzheimer's disease and their roles in AD pathogenesis and therapy.Medicinal research reviews · 2021Review
- Metformin prevents p-tau and amyloid plaque deposition and memory impairment in diabetic mice.Experimental brain research · 2021Article
- Exercise-Linked Irisin: Consequences on Mental and Cardiovascular Health in Type 2 Diabetes.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is progressive neurodegenerative disorder characterized by brain accumulation of the amyloid β peptide (Aβ), which form senile plaques, neurofibrillary tangles (NFT) and, eventually, neurodegeneration and cognitive impairment. Interestingly, epidemiological studies have described a relationship between type 2 diabetes mellitus (T2DM) and this pathology, being one of the risk factors for the development of AD pathogenesis. Information as it is, it would point out that, impairment in insulin signalling and glucose metabolism, in central as well as peripheral systems, would be one of the reasons for the cognitive decline. Brain insulin resistance, also known as Type 3 diabetes, leads to the increase of Aβ production and TAU phosphorylation, mitochondrial dysfunction, oxidative stress, protein misfolding, and cognitive impairment, which are all hallmarks of AD. Moreover, given the complexity of interlocking mechanisms found in late onset AD (LOAD) pathogenesis, more data is being obtained. Recent evidence showed that Aβ42 generated in the brain would impact negatively on the hypothalamus, accelerating the "peripheral" symptomatology of AD. In this situation, Aβ42 production would induce hypothalamic dysfunction that would favour peripheral hyperglycaemia due to down regulation of the liver insulin receptor. The objective of this review is to discuss the existing evidence supporting the concept that brain insulin resistance and altered glucose metabolism play an important role in pathogenesis of LOAD. Furthermore, we discuss AD treatment approaches targeting insulin signalling using anti-diabetic drugs and mTOR inhibitors.
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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.