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Research

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

Find studies

Showing 801–825 of 963 studies with an author at Harvard University (US) (page 33 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.

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.

Association between Hypothyroidism Onset and Alzheimer Disease Onset in Adults with Down Syndrome

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Brain sciences 2021-09-16

Adults with Down syndrome (DS) have an exceptionally high frequency of Alzheimer disease (AD) with a wide variability in onset, from 40 to 70 years of age. 2 key findings →

Participants: 232 Evidence: low

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

Age-dependent neuronal and synaptic degeneration in mice transgenic for the C terminus of the amyloid precursor protein

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 1996-11-01

The molecular basis for the degeneration of neurons and the deposition of amyloid in plaques and in the cerebrovasculature in Alzheimer's disease (AD) is incompletely understood. 4 key findings →

Evidence: low

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

Deficiency of Neuronal p38α MAPK Attenuates Amyloid Pathology in Alzheimer Disease Mouse and Cell Models through Facilitating Lysosomal Degradation of BACE1

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journal of biological chemistry 2015-12-09

Amyloid β (Aβ) damages neurons and triggers microglial inflammatory activation in the Alzheimer disease (AD) brain. 4 key findings →

Evidence: low

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

The amyloid precursor protein is concentrated in neuronal lysosomes in normal and Alzheimer disease subjects

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Experimental neurology 1989-12-01

The 4.2-kilodalton (kDa) polypeptide associated with the cerebral amyloid deposits of Alzheimer's disease (AD) derives from a much larger protein that is encoded by a gene on chromosome 21. 4 key findings →

Evidence: low

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

DNA synthesis and neuronal apoptosis caused by familial Alzheimer disease mutants of the amyloid precursor protein are mediated by the p21 activated kinase PAK3

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2003-07-01

Apoptotic pathways and DNA synthesis are activated in neurons in the brains of individuals with Alzheimer disease (AD). 4 key findings →

Evidence: low

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

Recommended best practices for construct-centered adaptation of the Harmonized Cognitive Assessment Protocol

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journals of Gerontology Series B 2025-10-24

Recommendations for HCAP adaptation include phases of preparation (assembling local expert teams; resource planning), implementation (construct-centered adaptation guided by local experts), pre-testing (iterative, mixed-methods approach), and field preparation (creating documentation; interviewer training; planning for ongoing quality assurance). 4 key findings →

Evidence: low

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

Type 2 diabetes and late-onset Alzheimer’s disease and related dementia: A longitudinal cohort study integrating polygenic risk score

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Journal of Alzheimer s Disease 2025-03-25

T2DM is one of the strong risk factors of ADRD but genetic T2DM effect does not contribute to ADRD risk. 3 key findings →

Evidence: moderate

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

Dissociable spatial topography of cortical atrophy in early‐onset and late‐onset Alzheimer's disease: A head‐to‐head comparison of the LEADS and ADNI cohorts

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Alzheimer s & Dementia 2025-02-01

After controlling for the level of cognitive impairment, we found a double dissociation between AD clinical phenotype and localization/magnitude of atrophy, characterized by predominant neocortical involvement in EOAD and more focal anterior medial temporal involvement in LOAD. 5 key findings →

Evidence: low

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

Better Assessment of Illness Study (BASIL) II for Delirium Severity: Study Design, Variables, and Methods

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Journal of Geriatric Psychiatry and Neurology 2025-05-16

PurposeDelirium is a common yet preventable complication of hospitalization, surgery and illness that is associated with poor outcomes. 1 key finding →

Design: cohort study Evidence: moderate

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

Retinal Imaging Findings in Carriers With PSEN1-Associated Early-Onset Familial Alzheimer Disease Before Onset of Cognitive Symptoms

✓ Peer-reviewed alzhub usefulness score 46 out of 100. JAMA ophthalmology 2021-01-01

These findings suggest that OCT can detect functional and morphologic changes in the retina of carriers of familial Alzheimer disease who are cognitively unimpaired several years before clinical onset, suggesting that OCT findings and retinal vascular parameters may be biomarkers prior to the onset of cognitive decline. 4 key findings →

Design: cross-sectional Evidence: low

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

Update on appropriate use criteria for amyloid PET imaging: dementia experts, mild cognitive impairment, and education

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of nuclear medicine : official publication, Society of Nuclear Medicine 2013-06-10

Amyloid PET imaging is a novel diagnostic test that can detect in living humans one of the two defining pathologic lesions of Alzheimer disease, amyloid-β deposition in the brain. 3 key findings →

Evidence: low

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

Neuropathology and apolipoprotein E profile of aged chimpanzees: implications for Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1994-09-01

Neuropathological findings in three aged chimpanzees were compared with those in rhesus monkeys and individuals with Alzheimer disease. 3 key findings →

Evidence: low

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

Frontotemporal and dopaminergic control of idea generation and creative drive

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of comparative neurology 2005-12-01

This article presents a three-factor anatomical model of human idea generation and creative drive, focusing on interactions between the temporal lobes, frontal lobes, and limbic system. 1 key finding →

Evidence: low

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

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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