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Research

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 76–100 of 118 studies with an author at Eli Lilly (United States) (US) (page 4 of 5) · 28,180 in the whole library · How the 0–100 score works

Download bibliography of these 118 studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Other institutions

From OpenAlex; 13,658 studies have no institution on record and are not counted here.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

Brain Imaging and Blood Biomarker Abnormalities in Children With Autosomal Dominant Alzheimer Disease: A Cross-Sectional Study

✓ Peer-reviewed alzhub usefulness score 55 out of 100. JAMA neurology 2015-08-01

Similar to findings in adult mutation carriers, in the later preclinical and clinical stages of ADAD, mutation-carrying children were distinguished from control individuals by significantly higher plasma Aβ1-42 levels (mean [SD]: carriers, 18.8 [5.1] pg/mL and noncarriers, 13.1 [3.2] pg/mL; P Conclusions and relevance Children at genetic risk for ADAD have functional and structural brain changes and abnormal levels of plasma Aβ1-42. 2 key findings →

Design: cross-sectional Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Alzheimer disease brain atrophy subtypes are associated with cognition and rate of decline

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Neurology 2017-10-25

An increased HV:CTV ratio was predictive of faster clinical decline in participants with AD who were clinically indistinguishable at baseline except for a greater dysexecutive presentation. 1 key finding →

Participants: 229 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

The Alzheimer's Disease Neuroimaging Initiative 3: Continued innovation for clinical trial improvement

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2016-12-05

ADNI-3 will aim to inform AD treatment trials and facilitate development of AD disease-modifying treatments. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Amyloid-related imaging abnormalities in amyloid-modifying therapeutic trials: Recommendations from the Alzheimer’s Association Research Roundtable Workgroup

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Alzheimer s & Dementia 2011-07-01

The Alzheimer's Association Research Roundtable convened a working group to review data on amyloid imaging related abnormalities (ARIA) in response to concerns raised by the Food and Drug Administration. 3 key findings →

Full summary, score breakdown and related studies → Original source Free full text

Plasma P-tau217 for detecting amyloid clearance after donanemab in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Alzheimer's & Dementia 2026-08-07

Despite reductions in plasma p-tau217 with donanemab treatment, this biomarker cannot currently be used to accurately detect TRAC by PET (< 24.1 CL) in individuals with early symptomatic AD. 1 key finding →

Design: phase-3-trial Participants: 830 Evidence: null result

Full summary, score breakdown and related studies → Original source Free full text

The Alzheimer's disease neuroimaging initiative: progress report and future plans

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2010-05-01

The Alzheimer's Disease Neuroimaging Initiative (ADNI) beginning in October 2004, is a 6-year research project that studies changes of cognition, function, brain structure and function, and biomarkers in elderly controls, subjects with mild cognitive impairment, and subjects with Alzheimer's disease (AD). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Genome-wide RNAseq study of the molecular mechanisms underlying microglia activation in response to pathological tau perturbation in the rTg4510 tau transgenic animal model

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Molecular neurodegeneration 2018-12-17

Activation of microglia, the resident immune cells of the central nervous system, is a prominent pathological hallmark of Alzheimer's disease (AD). 4 key findings →

Design: longitudinal study Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Apolipoprotein E promotes astrocyte colocalization and degradation of deposited amyloid-beta peptides

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Nature medicine 2004-06-13

We have previously shown that apolipoprotein E (Apoe) promotes the formation of amyloid in brain and that astrocyte-specific expression of APOE markedly affects the deposition of amyloid-beta peptides (Abeta) in a mouse model of Alzheimer disease. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Update on the biomarker core of the Alzheimer's Disease Neuroimaging Initiative subjects

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2010-05-01

Here, we review progress by the Penn Biomarker Core in the Alzheimer's Disease Neuroimaging Initiative (ADNI) toward developing a pathological cerebrospinal fluid (CSF) and plasma biomarker signature for mild Alzheimer's disease (AD) as well as a biomarker profile that predicts conversion of mild cognitive impairment (MCI) and/or normal control subjects to AD. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Combined Connectomics, MAPT Gene Expression, and Amyloid Deposition to Explain Regional Tau Deposition in Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Annals of neurology 2023-10-25

Across 3 study samples, combining the functional connectome and molecular properties substantially enhanced the explanatory power compared to single modalities, providing a valuable tool to explain regional susceptibility to tau deposition in AD. 3 key findings →

Participants: 1,000 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

A novel Abeta isoform pattern in CSF reflects gamma-secretase inhibition in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Alzheimer's research & therapy 2010-03-29

CSF Abeta1-14, Abeta1-15, and Abeta1-16 increase during gamma-secretase inhibitor treatment in AD, even at doses that do not affect Abeta1-42 or Abeta1-40, probably because of increased substrate availability of the C99 APP stub (APP beta-CTF) induced by gamma-secretase inhibition. 2 key findings →

Participants: 35 Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

Digital technologies as biomarkers, clinical outcomes assessment, and recruitment tools in Alzheimer's disease clinical trials

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Alzheimer's & dementia (New York, N. Y.) 2018-05-24

Digital technology is transforming the development of drugs for Alzheimer's disease and was the topic of the Alzheimer's Association's Research Roundtable on its May 23-24, 2017 meeting. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

TREM2 variants: new keys to decipher Alzheimer disease pathogenesis

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Nature reviews. Neuroscience 2016-02-25

Genome-wide association studies have identified rare variants of the gene that encodes triggering receptor expressed on myeloid cells 2 (TREM2) - an immune receptor that is found in brain microglia - as risk factors for non-familial Alzheimer disease (AD). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Predicting Short-term MCI-to-AD Progression Using Imaging, CSF, Genetic Factors, Cognitive Resilience, and Demographics

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Scientific reports 2019-02-19

In the Alzheimer's disease (AD) continuum, the prodromal state of mild cognitive impairment (MCI) precedes AD dementia and identifying MCI individuals at risk of progression is important for clinical management. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

New directions in clinical trials for frontotemporal lobar degeneration: Methods and outcome measures

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2020-01-06

New personalized endpoints that are clinically meaningful to individuals and their families should be developed. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

↑ Change the filters

Where “Free full text” comes from

Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read

How the 0–100 score works — and why some entries are capped

This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.

  • Journal tier up to 10 pts
  • Journal's citation record up to 4 pts
  • Study design up to 12 pts
  • Strength of evidence up to 5 pts
  • Peer-review validation up to 10 pts
  • How recent up to 5 pts
  • Sample size up to 4 pts
  • Effect reported up to 3 pts
  • Studied in people up to 3 pts
  • Randomised / blinded up to 2 pts
  • Times cited up to 7 pts
  • Citations per year up to 5 pts
  • Impact for its field and year up to 6 pts
  • Cited by studies here up to 6 pts
  • Still being cited up to 4 pts
  • Senior author's track record up to 4 pts
  • Institution's track record up to 3 pts
  • Multi-centre collaboration up to 3 pts
  • Indexed in PubMed up to 2 pts
  • Free to read up to 2 pts

Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.

Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.

We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.

The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.

See the whole rubric drawn out → — four charts covering all 28,180 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.

What this library is — and isn't

This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.

1,034 records (3.7% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.

See the full, machine-readable breakdown of this library's coverage →

Newest studies, as a dated timeline →    Atom feed