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Glial reaction in aging and Alzheimer's disease
Unger JW.. Microscopy research and technique, 1998-10-01
Topic: Amyloid, tau and blood-test diagnosis
It is well-established that glial cells play an important role during injury and neurodegenerative processes in the central nervous system. In normal aging, no global glia proliferation is found morphologically, but reactive gliosis has been described in specific areas of the limbic system and neocortex that undergo selective neuronal or synaptic degeneration in nondemented elderly persons. In addition, there is an age-associated increase in the metabolic turnover of cellular proteins, such as glial fibrillary acidic protein, in human brain tissue, even without detectable signs of neurodegeneration. In contrast to the relatively moderate overall glial changes in normal aging, the close association of activated astrocytes and microglial cells with neuritic plaques and cells undergoing neurofibrillary degeneration in Alzheimer's disease (AD), the expression of receptors for complement by glial cells, and the release of soluble cytokines strongly suggest that inflammatory processes may play an important part in the complex pathophysiological interactions that occur in AD. Understanding the role of glia in age-associated neurodegenerative disorders may provide new insights into the neurobiology of glia-neuronal interaction and may allow the development of strategies to alter the disease process. This review aims to summarize some of the important aspects of glial cells in aging and dementia.
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APA 7th
Unger, J. W. (1998). Glial reaction in aging and Alzheimer's disease. Microscopy research and technique. https://doi.org/10.1002/(sici)1097-0029(19981001)43:1<24::aid-jemt4>3.0.co;2-p
Vancouver
Unger JW. Glial reaction in aging and Alzheimer's disease. Microscopy research and technique. 1998. doi:10.1002/(sici)1097-0029(19981001)43:1<24::aid-jemt4>3.0.co;2-p. PMID: 9829455.
BibTeX
@article{unger1998-9829455,
author = {Unger, J. W.},
title = {{Glial reaction in aging and Alzheimer's disease}},
journal = {Microscopy research and technique},
year = {1998},
doi = {10.1002/(sici)1097-0029(19981001)43:1<24::aid-jemt4>3.0.co;2-p},
pmid = {9829455},
url = {https://doi.org/10.1002/(sici)1097-0029(19981001)43:1<24::aid-jemt4>3.0.co;2-p}
}
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Key findings
- In contrast to the relatively moderate overall glial changes in normal aging, the close association of activated astrocytes and microglial cells with neuritic plaques and cells undergoing neurofibrillary degeneration in Alzheimer's disease (AD), the expression of receptors for complement by glial cells, and the release of soluble cytokines strongly suggest that inflammatory processes may play an important part in the complex pathophysiological interactions that occur in AD.
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Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Microscopy research and technique) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 1998 — older than 20 years, still counted |
| 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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 9829455) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1002/(sici)1097-0029(19981001)43:1<24::aid-jemt4>3.0.co;2-p
- PubMed: 9829455
- Original source →
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