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Glutamatergic alterations and mitochondrial impairment in a murine model of Alzheimer disease
Cassano T, Serviddio G, Gaetani S, Romano A, Dipasquale P, Cianci S, Bellanti F, Laconca L et al.. Neurobiology of aging, 2011-10-27
Topic: Amyloid, tau and blood-test diagnosis
Deficits in glutamate neurotransmission and mitochondrial functions were detected in the frontal cortex (FC) and hippopcampus (HIPP) of aged 3×Tg-Alzheimer's disease (AD) mice, compared with their wild type littermates (non-Tg). In particular, basal levels of glutamate and vesicular glutamate transporter 1 (VGLUT1) expression were reduced in both areas. Cortical glutamate release responded to K(+) stimulation, whereas no peak release was observed in the HIPP of mutant mice. Synaptosomal-associated protein 25 (SNAP-25), glutamate/aspartate transporter (GLAST), glutamate transporter 1 (GLT1) and excitatory amino acid carrier 1 (EAAC1) were reduced in HIPP homogenates, where the adenosine triphosphate (ATP) content was lower. In contrast, glutamate transporter 1 and glial fibrillary acidic protein (GFAP) were found to be higher in the frontal cortex. The respiration rates of complex-I, II, IV, and the membrane potential were reduced in cortical mitochondria, where unaltered proton leak, F(0)F(1)-ATPase activity and ATP content, with increased hydrogen peroxide production (H(2)O(2)), were also observed. In contrast, complex-I respiration rate was significantly increased in hippocampal mitochondria, together with increased proton leak and H(2)O(2) production. Moreover, loss of complex-IV and F(0)F(1)-ATPase activities were observed. These data suggest that impairments of mitochondrial bioenergetics might sustain the failure in the energy-requiring glutamatergic transmission.
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APA 7th
Cassano, T., Serviddio, G., Gaetani, S., Romano, A., Dipasquale, P., Cianci, S., et al. (2012). Glutamatergic alterations and mitochondrial impairment in a murine model of Alzheimer disease. Neurobiology of aging. https://doi.org/10.1016/j.neurobiolaging.2011.09.021
Vancouver
Cassano T, Serviddio G, Gaetani S, Romano A, Dipasquale P, Cianci S, et al. Glutamatergic alterations and mitochondrial impairment in a murine model of Alzheimer disease. Neurobiology of aging. 2012. doi:10.1016/j.neurobiolaging.2011.09.021. PMID: 22035587.
BibTeX
@article{cassano2012-22035587,
author = {Cassano, T. and Serviddio, G. and Gaetani, S. and Romano, A. and Dipasquale, P. and Cianci, S. and Bellanti, F. and Laconca, L. and others},
title = {{Glutamatergic alterations and mitochondrial impairment in a murine model of Alzheimer disease}},
journal = {Neurobiology of aging},
year = {2012},
doi = {10.1016/j.neurobiolaging.2011.09.021},
pmid = {22035587},
url = {https://doi.org/10.1016/j.neurobiolaging.2011.09.021}
}
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Key findings
- Deficits in glutamate neurotransmission and mitochondrial functions were detected in the frontal cortex (FC) and hippopcampus (HIPP) of aged 3×Tg-Alzheimer's disease (AD) mice, compared with their wild type littermates (non-Tg).
- In contrast, complex-I respiration rate was significantly increased in hippocampal mitochondria, together with increased proton leak and H(2)O(2) production.
- These data suggest that impairments of mitochondrial bioenergetics might sustain the failure in the energy-requiring glutamatergic transmission.
Why it matters
In a mouse model of Alzheimer's disease, this study found deficits in glutamate neurotransmission and mitochondrial function in the frontal cortex and hippocampus. It is an animal study and does not test any treatment, cure or prevention in people.
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Study details
- Evidence strengthLow
How this study scored 41/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurobiology of aging) |
| Journal's citation record | 3 / 4 | Neurobiology of Aging: journal h-index 263 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2012 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Laboratory or animal study (title names “murine”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 98 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 6.1 citations a year over 16 year(s) since 2012 |
| Impact for its field and year | 3 / 6 | Cited 3.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 1 / 4 | Cited 13 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Gianluigi Vendemiale: h-index 66 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of California, Irvine: institution h-index 1,195 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 22035587) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 41 / 100 | — |
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