Home › Research › Brain scans and imaging
Does vascular pathology contribute to Alzheimer changes?
Kalaria RN, Akinyemi R, Ihara M.. Journal of the neurological sciences, 2012-08-11
Topic: Amyloid, tau and blood-test diagnosis
In recent years there has been increased interest in whether vascular disease contributes to Alzheimer's disease (AD). This review considers how modifiable risk factors such as hypertension, atherosclerosis, diabetes, dyslipidaemia and adiposity may impact on vascular structure and function to promote neurodegenerative processes and instigate AD. The presence of vascular pathology involving arterial stiffness, arteriolosclerosis, endothelial degeneration and blood-brain barrier dysfunction leads to chronic cerebral hypoperfusion. Pathological changes in human brain and animal studies suggest cerebral hypoperfusion which in turn induces several features of AD pathology including selective brain atrophy, white matter changes and accumulation of abnormal proteins such as amyloid β. Cerebral pathological changes may be further modified by genetic factors such as the apoliopoprotein E ε4 allele. Although tau hyperphosphorylation and tangle formation still needs robust explanation further support for the notion that vascular pathology influences AD changes is provided by the evidence that interventions which improve vascular function attenuate AD pathology.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Kalaria, R. N., Akinyemi, R., & Ihara, M. (2012). Does vascular pathology contribute to Alzheimer changes? Journal of the neurological sciences. https://doi.org/10.1016/j.jns.2012.07.032
Vancouver
Kalaria RN, Akinyemi R, Ihara M. Does vascular pathology contribute to Alzheimer changes? Journal of the neurological sciences. 2012. doi:10.1016/j.jns.2012.07.032. PMID: 22884479.
BibTeX
@article{kalaria2012-22884479,
author = {Kalaria, R. N. and Akinyemi, R. and Ihara, M.},
title = {{Does vascular pathology contribute to Alzheimer changes?}},
journal = {Journal of the neurological sciences},
year = {2012},
doi = {10.1016/j.jns.2012.07.032},
pmid = {22884479},
url = {https://doi.org/10.1016/j.jns.2012.07.032}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- This review considers how modifiable risk factors such as hypertension, atherosclerosis, diabetes, dyslipidaemia and adiposity may impact on vascular structure and function to promote neurodegenerative processes and instigate AD.
- The presence of vascular pathology involving arterial stiffness, arteriolosclerosis, endothelial degeneration and blood-brain barrier dysfunction leads to chronic cerebral hypoperfusion.
- Pathological changes in human brain and animal studies suggest cerebral hypoperfusion which in turn induces several features of AD pathology including selective brain atrophy, white matter changes and accumulation of abnormal proteins such as amyloid β.
- Cerebral pathological changes may be further modified by genetic factors such as the apoliopoprotein E ε4 allele.
- Although tau hyperphosphorylation and tangle formation still needs robust explanation further support for the notion that vascular pathology influences AD changes is provided by the evidence that interventions which improve vascular function attenuate AD pathology.
New to this subject? Start with our plain-English guide: Brain scans & tests →
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 (Journal of the neurological sciences) |
| 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 | 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 | 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 22884479) |
| 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
Free copy unknown: no free-copy check has an answer for this record yet. That does not mean it is paywalled.
Related studies in Brain scans and imaging
Also tagged “vascular-pathology”
2 studies in the library carry the topic tag “vascular-pathology”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 2 tagged studies.