ReviewPharmaceuticals (Basel, Switzerland)2022
Brain Glucose Hypometabolism and Iron Accumulation in Different Brain Regions in Alzheimer's and Parkinson's Diseases.
Review in Pharmaceuticals (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Safety and tolerability of intranasal insulin in Parkinson's disease.Frontiers in neurology · 2026Trial
- Omega-3 Fatty Acids and Alzheimer's Disease: Toward a New Understanding of Neuroprotective Mechanisms and Intervention Strategies.Marine drugs · 2026Review
- Allosteric Activation of GDH/TCA Pathway Reduces Pathological Build-Up and Promotes Neuronal Survival in an In Vitro Model of Alzheimer's Disease.Biomolecules · 2026Article
- Trends and challenges in imaging research of Parkinson's disease: a 10-year bibliometric analysis.Psychoradiology · 2026Article
- New Approaches and Strategies for the Repurposing of Iron Chelating/Antioxidant Drugs for Diseases of Free Radical Pathology in Medicine.Antioxidants (Basel, Switzerland) · 2025Review
- Metabolic Dysregulation in Parkinson's Disease: Non-Oxidative Phosphorylation and Its Role in Brain Energy Metabolism.Aging and disease · 2025Review
- Abnormal iron metabolism in the zona incerta in Parkinson's disease mice.Journal of neural transmission (Vienna, Austria : 1996) · 2025Article
- Understanding Causal Relationships Between Imaging-Derived Phenotypes and Parkinson's Disease: A Mendelian Randomization and Observational Study.Biomedicines · 2025Article
- Brain Glucose Hypometabolism and Brain Iron Accumulation as Therapeutic Targets for Alzheimer's Disease and Other CNS Disorders.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Altered frontotemporal glucose metabolism following radiotherapy and/or chemotherapy for cervical cancer.Frontiers in neurology · 2025Article
- Distinct regional vulnerability to Aβ and iron accumulation in post mortem AD brains.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Iron accumulation/overload and Alzheimer's disease risk factors in the precuneus region: A comprehensive narrative review.Aging medicine (Milton (N.S.W)) · 2024Review
- Review
- The characteristic patterns of individual brain susceptibility networks underlie Alzheimer's disease and white matter hyperintensity-related cognitive impairment.Translational psychiatry · 2024Article
- Low-dose intranasal deferoxamine modulates memory, neuroinflammation, and the neuronal transcriptome in the streptozotocin rodent model of Alzheimer's disease.Frontiers in neuroscience · 2024Article
- Evaluating iron deposition in gray matter nuclei of patients with acute ischemic stroke using quantitative susceptibility mapping.Frontiers in neurology · 2024Article
- Correlation of brain iron deposition and freezing of gait in Parkinson's disease: a cross-sectional study.Quantitative imaging in medicine and surgery · 2023Article
- Review
- Brain iron content in cerebral amyloid angiopathy using quantitative susceptibility mapping.Frontiers in neuroscience · 2023Article
- Regional high iron deposition on quantitative susceptibility mapping correlates with cognitive decline in type 2 diabetes mellitus.Frontiers in neuroscience · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to examine the relationship between the presence of glucose hypometabolism (GHM) and brain iron accumulation (BIA), two potential pathological mechanisms in neurodegenerative disease, in different regions of the brain in people with late-onset Alzheimer's disease (AD) or Parkinson's disease (PD). Studies that conducted fluorodeoxyglucose positron emission tomography (FDG-PET) to map GHM or quantitative susceptibility mapping-magnetic resonance imaging (QSM-MRI) to map BIA in the brains of patients with AD or PD were reviewed. Regions of the brain where GHM or BIA were reported in each disease were compared. In AD, both GHM and BIA were reported in the hippocampus, temporal, and parietal lobes. GHM alone was reported in the cingulate gyrus, precuneus and occipital lobe. BIA alone was reported in the caudate nucleus, putamen and globus pallidus. In PD, both GHM and BIA were reported in thalamus, globus pallidus, putamen, hippocampus, and temporal and frontal lobes. GHM alone was reported in cingulate gyrus, caudate nucleus, cerebellum, and parietal and occipital lobes. BIA alone was reported in the substantia nigra and red nucleus. GHM and BIA are observed independent of one another in various brain regions in both AD and PD. This suggests that GHM is not always necessary or sufficient to cause BIA and vice versa. Hypothesis-driven FDG-PET and QSM-MRI imaging studies, where both are conducted on individuals with AD or PD, are needed to confirm or disprove the observations presented here about the potential relationship or lack thereof between GHM and BIA in AD and PD.
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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.