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Find studies

Showing 876–900 of 963 studies with an author at Harvard University (US) (page 36 of 39) · 28,180 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these 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.

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.

The machine learning model predicted MMSE scores with a root-mean-squared error (RMSE) of 2.43 in the BH test set. 4 key findings →

Participants: 945 Evidence: moderate

Tumor necrosis factor (TNF), a proinflammatory cytokine, may be involved in the pathogenesis of Alzheimer disease (AD) based on observations that senile plaques have been found to upregulate proinflammatory cytokines. 3 key findings →

Evidence: low

We review the changing conceptions of schizophrenia over the past 50 years as it became understood as a disorder of brain function and structure in which neurocognitive dysfunction was identified at different illness phases. 2 key findings →

Evidence: low

Biological effects related to cell growth, as well as a role in the pathogenesis of Alzheimer disease, have been ascribed to the beta-amyloid precursor protein (beta-APP). 4 key findings →

Evidence: low

A G-rich element forms a G-quadruplex and regulates BACE1 mRNA alternative splicing

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Journal of neurochemistry 2012-03-13

β-Site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) is the transmembrane aspartyl protease that catalyzes the first cleavage step in the proteolysis of the APP to the amyloid β-protein (Aβ), a process involved in the pathogenesis of Alzheimer disease. 4 key findings →

Evidence: low

The spreading of MAPT/Tau pathology is closely associated with the progression of neurodegeneration and cognitive decline in Alzheimer disease and other tauopathies. 5 key findings →

Evidence: low

Familial Alzheimer's disease (FAD) is caused by dominant missense mutations in amyloid precursor protein (APP) and presenilin-1 (PSEN1), the catalytic component of γ-secretase that generates amyloid β-peptides (Aβ) from the APP C-terminal fragment C99. 3 key findings →

Evidence: low

It has been demonstrated to have neuroprotective effects in cellular models of neurodegenerative diseases; however, its precise mechanism of action in alleviating tau pathology in Alzheimer's disease (AD), as well as its potential to improve cognitive deficits in animal models, has not yet been elucidated. 3 key findings →

Evidence: low

Our findings suggest that quantification of WM changes in DS could provide a promising and clinically relevant biomarker for AD clinical onset and progression. 2 key findings →

Evidence: low

Of 2 197 732 beneficiaries enrolled in D-SNPs in 2021, 881 736 (40.1%) were living in counties with aligned enrollment available and 251 305 (11.4%) enrolled. 5 key findings →

Evidence: low

We found 5 distinct clusters of subjects (N=38, N=16, N=24, N=14, N=21) with a composition statistically independent from that obtained using available clinical diagnostic criteria (each cluster included all phenotypical groups). 3 key findings →

Participants: 20 Evidence: moderate

A total of 85 patients were included in the study with rare genotypes excluded from analysis (3 patients). 5 key findings →

Participants: 85 Evidence: moderate

Diet and Prevention of Cardiovascular Disease and Cancer

✓ Peer-reviewed alzhub usefulness score 41 out of 100. JACC CardioOncology 2025-08-29

Cardiovascular disease (CVD) and cancer remain the leading causes of mortality in the United States, where poor diet has surpassed smoking as the leading risk factor for death, and life expectancy has hit a plateau as CVD mortality has stagnated over the past decade. 1 key finding →

Evidence: low

RoCA classifies patients similarly to gold standard paper-based tests, with a receiver operating characteristic area under the curve of 0.81 (95% CI 0.67-0.91; P<.001). 5 key findings →

Design: open-label trial Participants: 35 Evidence: low

BackgroundClinician communication at the time of a dementia diagnosis often inadequately addresses patient and caregiver needs. 5 key findings →

Participants: 21 Evidence: low

Vascular cognitive impairment and dementia (VCID) encompasses a heterogeneous group of disorders in which cerebrovascular pathology contributes to cognitive decline. 2 key findings →

Evidence: low

Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy associated with repetitive head impact (RHI) exposure. 3 key findings →

Evidence: low

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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