The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.
Brain Glucose Hypometabolism and Oxidative Stress in Preclinical Alzheimer's Disease
Open accessAbstract
One of the main features of Alzheimer's disease (AD) is the severe reduction of the cerebral metabolic rate for glucose (CMRglc). In vivo imaging using positron emission tomography with 2‐[ 18 F]fluoro‐2‐deoxy‐D‐glucose (FDG–PET) demonstrates consistent and progressive CMRglc reductions in AD patients, the extent and topography of which correlate with symptom severity. Increasing evidence suggests that CMRglc reductions occur at the preclinical stages of AD. CMRglc reductions were observed on FDG–PET before the onset of disease in several groups of at‐risk individuals, including patients with mild cognitive impairment (MCI), often a prodrome to AD; presymptomatic individuals carrying mutations responsible for early‐onset familial AD; cognitively normal elderly individuals followed for several years until they declined to MCI and eventually to AD; normal, middle‐aged individuals who expressed subjective memory complaints and were carriers of the apolipoprotein E epsilon‐4 allele, a strong genetic risk factor for late‐onset AD. However, the causes of the early metabolic dysfunction forerunning the onset of AD are not known. An increasing body of evidence indicates a deficient or altered energy metabolism that could change the overall oxidative microenvironment for neurons during the pathogenesis and progression of AD, leading to alterations in mitochondrial enzymes and in glucose metabolism in AD brain tissue. The present paper reviews findings that implicate hypometabolism and oxidative stress as crucial players in the initiation and progression of synaptic pathology in AD.
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Cites
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Cited by
Brain energy metabolism: focus on Astrocyte-neuron metabolic cooperation
Bélanger, M., Allaman, I., & Magistretti, P. J. (2011) · Cell Metabolism · doi:10.1016/j.cmet.2011.08.016 · Cited by 2,313
Oxidative Stress, Synaptic Dysfunction, and Alzheimer’s Disease
Tönnies, E., & Trushina, E. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-161088 · Cited by 1,750
Is Alzheimer’s disease a type 3 diabetes? A critical appraisal
Kandimalla, R., Thirumala, V., & Reddy, P. H. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2016.08.018 · Cited by 621
Butyrate, neuroepigenetics and the gut microbiome: Can a high fiber diet improve brain health?
Bourassa, M. W., Alim, I., Bultman, S. J., & Ratan, R. R. (2016) · Neuroscience Letters · doi:10.1016/j.neulet.2016.02.009 · Cited by 632
González-Reyes, R. E., Nava-Mesa, M. O., Vargas-Sánchez, K., Ariza-Salamanca, D., & Mora-Muñoz, L. (2017) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2017.00427 · Cited by 527
Metadata
- Authors
- Mosconi, L., Pupi, A., & De Leon, M. J.
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2008-12
- Volume
- 1147
- Issue
- 1
- Pages
- 180-195
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- OpenAlex
- W2031155126
- Cited by
- 595
- References
- 29
- FWCI
- 13.47
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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