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Endogenous Lithium Levels and Alzheimer Disease
Raymond T. Suhandynata, Elizabeth A. Bevins, Imir G. Metushi. Clinical Chemistry, 2025-11-21
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer disease (AD) is the most common cause of dementia and the sixth leading cause of death among adults ≥65 years in the United States (1). By 2060, approximately 14 million Americans are projected to have AD, and twice as many may have mild cognitive impairment (1). In 2025, the total cost of caring for patients with dementia is estimated at $384 billion. This is predicted to rise toward about $1 trillion over the next three decades (1). The pathophysiology of AD remains poorly understood, with multifactorial etiology (age, genetics, environmental, and lifestyle factors). AD is histologically characterized by β-amyloid deposition and pathologic tau protein in the brain. It is currently diagnosed by cerebrospinal fluid biomarkers (total tau, phosphorylated tau, and amyloid-β42); positron emission tomography (amyloid or tau); or the newly FDA-approved blood tests (Lumipulse G pTau217/β-amyloid 1–42 plasma ratio and Elecsys pTau181). Current AD therapies are limited. Cholinesterase inhibitors offer modest cognitive benefit, and newly approved anti-amyloid antibody infusions slow mild-stage progression by approximately 30% but carry the risk of serious adverse effects (1). With most AD drugs trials failing, a substantial unmet therapeutic need remains.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Suhandynata, R. T., Bevins, E. A., & Metushi, I. G. (2025). Endogenous Lithium Levels and Alzheimer Disease. Clinical Chemistry. https://doi.org/10.1093/clinchem/hvaf174
Vancouver
Suhandynata RT, Bevins EA, Metushi IG. Endogenous Lithium Levels and Alzheimer Disease. Clinical Chemistry. 2025. doi:10.1093/clinchem/hvaf174. PMID: 41784383.
BibTeX
@article{suhandynata2025-41784383,
author = {Suhandynata, Raymond T. and Bevins, Elizabeth A. and Metushi, Imir G.},
title = {{Endogenous Lithium Levels and Alzheimer Disease}},
journal = {Clinical Chemistry},
year = {2025},
doi = {10.1093/clinchem/hvaf174},
pmid = {41784383},
url = {https://doi.org/10.1093/clinchem/hvaf174}
}
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
- The pathophysiology of AD remains poorly understood, with multifactorial etiology (age, genetics, environmental, and lifestyle factors).
- AD is histologically characterized by β-amyloid deposition and pathologic tau protein in the brain.
- It is currently diagnosed by cerebrospinal fluid biomarkers (total tau, phosphorylated tau, and amyloid-β42); positron emission tomography (amyloid or tau); or the newly FDA-approved blood tests (Lumipulse G pTau217/β-amyloid 1–42 plasma ratio and Elecsys pTau181).
- Cholinesterase inhibitors offer modest cognitive benefit, and newly approved anti-amyloid antibody infusions slow mild-stage progression by approximately 30% but carry the risk of serious adverse effects (1).
- With most AD drugs trials failing, a substantial unmet therapeutic need remains.
Why it matters
This text notes that current Alzheimer's therapies are limited, with cholinesterase inhibitors offering modest cognitive benefit and newly approved anti-amyloid antibody infusions slowing mild-stage progression by about 30% while carrying risk of serious adverse effects. It states that most Alzheimer's drug trials have failed and a substantial unmet therapeutic need remains.
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Study details
- Evidence strengthLow
How this study scored 31/100
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Clinical Chemistry) |
| Journal's citation record | 3 / 4 | Clinical Chemistry: journal h-index 323 (OpenAlex, 2026-10-29) |
| 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 | 4 / 5 | 2025 — within 3 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 | 0 / 7 | Cited 0 times (OpenAlex, 2026-10-10) |
| Citations per year | 0 / 5 | 0.0 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 0 / 6 | Cited 0.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 0 / 4 | Cited 0 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 1 / 4 | Last-listed author Imir G. Metushi: h-index 17 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of California, Los Angeles: institution h-index 1,923 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 41784383) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 31 / 100 | — |
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