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Endosome function and dysfunction in Alzheimer's disease and other neurodegenerative diseases
Nixon RA.. Neurobiology of aging, 2005-03-01
Topic: Disease mechanisms in lab and animal studies
Endocytosis is universally important in cell function. In the brain, the roles of endosomes are relatively more complex due to the unique polar morphology of neurons and specialized needs for inter-cellular communication. New evidence shows that endosome function is altered in a surprising range of neurodegenerative disorders, including in several inherited neurologic disorders where the causative mutations occur in genes that regulate endosome function. In Alzheimer's disease (AD), endosome abnormalities are among the earliest neuropathologic features to develop and have now been closely linked to genetic risk factors for AD, including APP triplication in Trisomy 21 (Down syndrome, DS) and ApoE4 genotype in sporadic AD. Recent findings on endosome regulation and developmental and late-onset neurodegenerative disease disorders are beginning to reveal how endocytic pathway impairment may lead to neuronal dysfunction and cell death in these disorders and may also promote amyloidogenesis in AD.
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APA 7th
Nixon, R. A. (2005). Endosome function and dysfunction in Alzheimer's disease and other neurodegenerative diseases. Neurobiology of aging. https://doi.org/10.1016/j.neurobiolaging.2004.09.018
Vancouver
Nixon RA. Endosome function and dysfunction in Alzheimer's disease and other neurodegenerative diseases. Neurobiology of aging. 2005. doi:10.1016/j.neurobiolaging.2004.09.018. PMID: 15639316.
BibTeX
@article{nixon2005-15639316,
author = {Nixon, R. A.},
title = {{Endosome function and dysfunction in Alzheimer's disease and other neurodegenerative diseases}},
journal = {Neurobiology of aging},
year = {2005},
doi = {10.1016/j.neurobiolaging.2004.09.018},
pmid = {15639316},
url = {https://doi.org/10.1016/j.neurobiolaging.2004.09.018}
}
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Key findings
- Endocytosis is universally important in cell function.
- In the brain, the roles of endosomes are relatively more complex due to the unique polar morphology of neurons and specialized needs for inter-cellular communication.
- New evidence shows that endosome function is altered in a surprising range of neurodegenerative disorders, including in several inherited neurologic disorders where the causative mutations occur in genes that regulate endosome function.
- In Alzheimer's disease (AD), endosome abnormalities are among the earliest neuropathologic features to develop and have now been closely linked to genetic risk factors for AD, including APP triplication in Trisomy 21 (Down syndrome, DS) and ApoE4 genotype in sporadic AD.
- Recent findings on endosome regulation and developmental and late-onset neurodegenerative disease disorders are beginning to reveal how endocytic pathway impairment may lead to neuronal dysfunction and cell death in these disorders and may also promote amyloidogenesis in AD.
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 (Neurobiology of aging) |
| 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 | 2005 — 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 15639316) |
| 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 | — |
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