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Research

28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 10,201–10,225 of 16,065 studies scoring 30–49 out of 100 (page 409 of 643) · 28,980 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.

Institutions

From OpenAlex; 14,457 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.

Cognitive and neurologic findings in subjects with diffuse white matter lucencies on computed tomographic scan (leuko-araiosis)

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Archives of neurology 1987-01-01

As part of a prospective clinicopathologic study, a cohort of 105 "normal" elderly volunteers was investigated with computed tomographic scans, psychometric testing (Extended Scale for Dementia [ESD]) and neurologic examination. 3 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source

Disease-specific patterns of locus coeruleus cell loss

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Annals of neurology 1992-11-01

Computer visualization techniques were used to map and to quantitatively reconstruct the entire locus coeruleus, including the nucleus subcoeruleus, to compare the topographic patterns of cell loss in postmortem brains from patients with Parkinson's disease, Alzheimer's disease, and Down syndrome. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Introduction and expression of the 400 kilobase amyloid precursor protein gene in transgenic mice [corrected]

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Nature genetics 1993-09-01

Overexpression of the gene encoding the beta-amyloid precursor protein (APP) may have a key role in the pathogenesis of both Alzheimer's disease (AD) and Down Syndrome (DS). 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

DYRK1A, a Dosage-Sensitive Gene Involved in Neurodevelopmental Disorders, Is a Target for Drug Development in Down Syndrome

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Frontiers in behavioral neuroscience 2016-06-03

Down syndrome (DS) is one of the leading causes of intellectual disability, and patients with DS face various health issues, including learning and memory deficits, congenital heart disease, Alzheimer's disease (AD), leukemia, and cancer, leading to huge medical and social costs. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Down syndrome--recent progress and future prospects

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Human molecular genetics 2009-04-01

Down syndrome (DS) is caused by trisomy of chromosome 21 (Hsa21) and is associated with a number of deleterious phenotypes, including learning disability, heart defects, early-onset Alzheimer's disease and childhood leukaemia. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Amyloid beta protein (Abeta) deposition in chromosome 14-linked Alzheimer's disease: predominance of Abeta42(43)

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Annals of neurology 1996-08-01

Amyloid beta protein (Abeta) deposition was investigated in the frontal cortex of 8 cases of (genetically confirmed) chromosome 14-linked Alzheimer's disease (AD) using the end-specific monoclonal antibodies BA27 and BC05 to detect the presence of Abeta40 and Abeta42(43), respectively. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Huntington's disease: from molecular pathogenesis to clinical treatment

✓ Peer-reviewed alzhub usefulness score 40 out of 100. The Lancet. Neurology 2011-01-01

Huntington's disease is a progressive, fatal, neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin gene, which encodes an abnormally long polyglutamine repeat in the huntingtin protein. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Cognitive impairment in Parkinson's disease: the dual syndrome hypothesis

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neuro-degenerative diseases 2012-10-03

Research into the heterogeneous nature of cognitive impairment documented in patients with Parkinson's disease (PD) has focused on disentangling deficits that vary between individuals, evolve and respond differentially to pharmacological treatments, and relate differentially to PD dementia (PDD). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

AGGRESCAN: a server for the prediction and evaluation of "hot spots" of aggregation in polypeptides

✓ Peer-reviewed alzhub usefulness score 40 out of 100. BMC bioinformatics 2007-02-27

By identifying aggregation-prone segments in proteins, AGGRESCAN http://bioinf.uab.es/aggrescan/ shall facilitate (i) the identification of possible therapeutic targets for anti-depositional strategies in conformational diseases and (ii) the anticipation of aggregation phenomena during storage or recombinant production of bioactive polypeptides or polypeptide sets. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Altered expression of synaptic proteins occurs early during progression of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neurology 2001-01-01

The expression levels of three synaptic proteins (synaptophysin, synaptotagmin, and growth-associated protein 43 [GAP43]) in AD cases clinically classified by Clinical Dementia Rating (CDR) score were analyzed. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

A High-Throughput Drug Screening Assay for Anti-Tau Aggregation Using Split GFP and Flow Cytometry

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Scientific reports 2025-06-18

Tau protein aggregation is a hallmark of neurodegenerative diseases, including Alzheimer's disease, making the development of anti-aggregation therapeutics a critical area of research. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Impaired BDNF-TrkB trafficking and signalling in Down syndrome basal forebrain neurons

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Cell death & disease 2025-07-18

Brain derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase B (TrkB) play crucial roles in neuronal development, synaptic transmission, and neuroplasticity. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

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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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.

1,038 records (3.6% of the library) are not peer-reviewed — 966 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