Evidence mapPaperPMID 41718800Full record

ArticleJournal of molecular neuroscience : MN2026

Higher Serum Levels of Propionylcarnitine and Methionine are Associated with Reduced Cortical Amyloid Burden in Alzheimer's Disease.

Qamar Abuhassan, Ghaleb Oriquat, Soumya V Menon, Laxmidhar Maharana, L Inbathamizh, Gunjan Mukherjee, Aashna Sinha, Shokhjakhon Furkatov, Alzheimer’s Disease Neuroimaging Initiative (ADNI) and the Alzheimer Disease Metabolomics Consortium (ADMC)

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular neuroscience : MN, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Qamar AbuhassanDepartment of Pharmaceutics and Pharmaceutical Technology, School of Pharmacy, University of Jordan, Amman, 11942, Jordan.
Ghaleb OriquatFaculty of Allied Medical Sciences, Hourani Center for Applied Scientific Research, Al- Ahliyya Amman University, Amman, Jordan. goreqat@ammanu.edu.jo.
Soumya V MenonDepartment of Chemistry and Biochemistry, School of Sciences, JAIN (Deemed to be University), Bangalore, Karnataka, India.
Laxmidhar MaharanaDepartment of Pharmaceutical Sciences, Siksha 'O' Anusandhan (Deemed to be University), Bhubaneswar, 751030, Odisha, India.
L InbathamizhDepartment of Biotechnology, Sathyabama Institute of Science and Technology, Chennai, Tamil Nadu, India.
Gunjan MukherjeeUniversity Institute of Biotechnology, Chandigarh University, Mohali, Punjab, India.
Aashna SinhaSchool of Applied and Life Sciences, Division of Research and Innovation, Uttaranchal University, Dehradun, Uttarakhand, India.
Shokhjakhon FurkatovDepartment of Oral Surgery and Dental Implantology, Samarkand State Medical University, Samarkand, Uzbekistan.
Alzheimer’s Disease Neuroimaging Initiative (ADNI) and the Alzheimer Disease Metabolomics Consortium (ADMC)

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered systemic metabolism contributes to Alzheimer’s disease (AD) pathology, yet the links between specific metabolites, cortical amyloid deposition, and cognition remain unclear. This study conducted targeted profiling of over 600 serum metabolites across 26 biochemical classes in 746 ADNI participants (CN = 248, MCI = 403, AD = 95), identifying propionylcarnitine and methionine as significantly associated metabolites. Relationships among these metabolites, cortical Aβ accumulation, and cognitive performance were examined using regression and mediation analyses, adjusting for age, sex, education, and APOE ε4 status. The results showed that serum propionylcarnitine and methionine levels did not differ across diagnostic groups. In AD participants, higher propionylcarnitine (β = − 0.24, FDR p = 0.019) and methionine (β = − 0.33, FDR p = 0.005) levels were associated with lower cerebellum-referenced cortical amyloid burden, whereas no significant associations were observed in CN or MCI individuals. Mediation analyses indicated that serum propionylcarnitine did not show significant indirect effects on cognitive performance via cortical amyloid burden in any group. For methionine, nominally significant indirect effects on cognition were observed in AD participants before FDR correction (ADAS-Cog 11: β = − 0.11, p = 0.040; ADAS-Cog 13: β = − 0.13, p = 0.044), but these did not remain significant after FDR adjustment (FDR p > 0.19), suggesting modest, non-significant associations of methionine with cognitive performance via cortical amyloid burden, although these findings were observational and did not imply causation. In short, higher propionylcarnitine and methionine were linked to lower cortical Aβ accumulation in AD, highlighting future research directions to explore their mechanistic roles in AD pathology.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesCarnitineCerebral CortexMethionineAgedAged, 80 and overBiomarkersCognitive DysfunctionFemaleHumansMaleAmyloid beta-PeptidesBiomarkersCarnitineMethioninepropionylcarnitineAlzheimer’s diseaseCognitionCortical amyloidMethioninePropionylcarnitineSerum metabolomics

Identifiers

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.