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Systemic and central nervous system metabolic alterations in Alzheimer's disease
van der Velpen V, Teav T, Gallart-Ayala H, Mehl F, Konz I, Clark C, Oikonomidi A, Peyratout G et al.. Alzheimer's research & therapy, 2019-11-28
Topic: Gut, metabolism and diet
The observed metabolic alterations were associated with core pathological processes of AD to investigate their relation with amyloid pathology and tau-related neurodegeneration. Results Concentrations of several TCA cycle and beta-oxidation intermediates were higher in plasma of AD patients, whilst amino acid concentrations were significantly lower. Alterations of several amino acids were associated with CSF Amyloidβ1-42. The tryptophan catabolites, kynurenic acid and quinolinic acid, showed significantly higher concentrations in CSF of AD patients, which, together with other tryptophan pathway intermediates, were correlated with either CSF Amyloidβ1-42, or tau and phosphorylated Tau-181. Conclusions This study revealed AD-associated systemic dysregulation of nutrient sensing and oxidation and CNS-specific alterations in the neuroactive tryptophan pathway and (phospho)creatine degradation. Our findings warrant validation in independent, larger cohort studies as well as further investigation of factors such as gender and APOE genotype, as well as of other groups, such as preclinical AD, to identify metabolic alterations as potential intervention targets.
Key findings
- The observed metabolic alterations were associated with core pathological processes of AD to investigate their relation with amyloid pathology and tau-related neurodegeneration.
- Results Concentrations of several TCA cycle and beta-oxidation intermediates were higher in plasma of AD patients, whilst amino acid concentrations were significantly lower.
- Alterations of several amino acids were associated with CSF Amyloidβ1-42.
- The tryptophan catabolites, kynurenic acid and quinolinic acid, showed significantly higher concentrations in CSF of AD patients, which, together with other tryptophan pathway intermediates, were correlated with either CSF Amyloidβ1-42, or tau and phosphorylated Tau-181.
- Conclusions This study revealed AD-associated systemic dysregulation of nutrient sensing and oxidation and CNS-specific alterations in the neuroactive tryptophan pathway and (phospho)creatine degradation.
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Study details
- Study designcohort study
- Participants40
- Evidence strengthModerate
How this study scored 64/100
Published in a peer-reviewed journal, and it is a cohort study following people over time. Scored zero for effect reported 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 37 of the 58 points we could judge it on, which is 64 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Alzheimer's research & therapy) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 7 / 12 | A cohort study following people over time |
| Strength of evidence | 3 / 5 | Rated “moderate” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2019 — within 10 year(s) of the newest study here |
| Sample size | 1 / 4 | 40 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| 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 31779690) |
| Free to read | 2 / 2 | Free to read |
| Points | 37 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 37 of the 58 points we could judge it on is 64 out of 100. |
| Total | 64 / 100 | — |
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APA 7th
van der Velpen, V., Teav, T., Gallart-Ayala, H., Mehl, F., Konz, I., Clark, C., et al. (2019). Systemic and central nervous system metabolic alterations in Alzheimer's disease. Alzheimer's research & therapy. https://doi.org/10.1186/s13195-019-0551-7
Vancouver
van der Velpen V, Teav T, Gallart-Ayala H, Mehl F, Konz I, Clark C, et al. Systemic and central nervous system metabolic alterations in Alzheimer's disease. Alzheimer's research & therapy. 2019. doi:10.1186/s13195-019-0551-7. PMID: 31779690.
BibTeX
@article{vandervelpen2019-31779690,
author = {van der Velpen, V. and Teav, T. and Gallart-Ayala, H. and Mehl, F. and Konz, I. and Clark, C. and Oikonomidi, A. and Peyratout, G. and others},
title = {{Systemic and central nervous system metabolic alterations in Alzheimer's disease}},
journal = {Alzheimer's research \& therapy},
year = {2019},
doi = {10.1186/s13195-019-0551-7},
pmid = {31779690},
url = {https://doi.org/10.1186/s13195-019-0551-7}
}