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Find studies

Showing 26,376–26,400 of 27,146 studies marked Peer-reviewed (page 1056 of 1086) · 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 socio-economic determinants of COVID-19: A spatial analysis of German county level data

✓ Peer-reviewed alzhub usefulness score 33 out of 100. Not indexed 2020-07-07

The case and death rates are, for example, significantly positively associated with early cases from the beginning of the epidemic, the average age, the population density and the number of people employed in elderly care. 4 key findings →

Evidence: low

The prevalence of hypertension showed statistically significant spatial clustering (global Moran’s I=0.442, p<.001), with high-high clusters concentrated in rural eup-myeon areas and low-low clusters in urban dong areas. 4 key findings →

Participants: 62,411 Evidence: low

Our case series highlighted the relevance of neurological comorbidities in BP patients; although the pathogenesis is still to be elucidated, the neuroinflammation present in neurodegenerative diseases could explain the neurocutaneous link and the chronological relationship between these entities. 3 key findings →

Participants: 257 Evidence: low

Alzheimer's Disease is Type 3 Diabetes-Evidence Reviewed

✓ Peer-reviewed alzhub usefulness score 32 out of 100. Journal of Diabetes Science and Technology 2008-11

This influential review article proposed that Alzheimer's disease could be considered a brain-specific form of diabetes, arguing that impaired insulin and insulin-like growth factor signaling in the brain drives amyloid buildup, tau tangles, oxidative stress, and energy failure - the hallmark features of Alzheimer's - and coined the term 'type 3 diabetes' for this concept. 4 key findings →

Evidence: preliminary

Glial HO-1 expression, iron deposition and oxidative stress in neurodegenerative diseases

✓ Peer-reviewed alzhub usefulness score 32 out of 100. Neurotoxicity research 1999-09-01

The mechanisms responsible for the pathological deposition of brain iron in Parkinson's disease, Alzheimer's disease and other human neurodegenerative disorders remain poorly understood. 2 key findings →

Evidence: low

Immunocytochemical techniques was used to compare the proportion of neurons expressing various neurotransmitters (tyrosine hydroxylase, choline acetyltransferase and gamma-aminobutyric acid), neuropeptides (Leu-enkephalin and substance P) and neural cell adhesion molecules (NCAM) in the hippocampus, frontal (area 10) and occipital (area 17) cortices of neurologically normal elderly humans to that of age-matched Alzheimer disease (AD) patients. 3 key findings →

Evidence: low

Features of multipotentiality of engineered NSC-derived cell lines versus naive cells (control-NSC) were assessed by immunocytochemical analysis in differentiation conditions. 5 key findings →

Evidence: low

Attitudes towards euthanasia among physicians, nurses and the general public in Finland

✓ Peer-reviewed alzhub usefulness score 32 out of 100. Public health 2002-11-01

The object of this study was to investigate the attitudes of physicians, nurses and the general public to physician-assisted suicide (PAS), active voluntary euthanasia (AVE) and passive euthanasia (PE) in Finland. 1 key finding →

Evidence: low

The internal consistency (Cronbach's alpha) of the ADAS-cog were 0.91, 0.88 and 0.65 for the whole group, the AD and normal (i.e. non-demented) subjects respectively. 1 key finding →

Evidence: low

On the basis of what is known about the neural circuitry essential or normally involved in eyeblink classical conditioning (EBCC), the pattern of neurodegeneration in Huntington's disease (HD) would not appear to interfere with this type of learning. 3 key findings →

Evidence: low

Immunohistochemical staining with polyclonal antibodies to synthetic amyloid (residues 1-28 of A4) was performed on normal and Down syndrome brains from fetuses to adults. 1 key finding →

Evidence: low

The present findings demonstrate several fundamental parallels between lens and neuron vesicle trafficking cell biology and development, and suggest that more extensive AbetaPP related vesicle trafficking disease mechanisms may be shared by lens and brain. 4 key findings →

Evidence: low

Immunoreactivity of presenilin-1 in human, rat and mouse brain

✓ Peer-reviewed alzhub usefulness score 32 out of 100. Brain research 1997-05-01

Monoclonal antibodies (mAbs) D3G6 and C8A5, specific for amino acid residues 160-168 of S182 protein, immunolabeled neurons, ependymal and choroid plexus cells, and myocytes in brain sections from normal subjects and people with Alzheimer disease or Down syndrome and in rats and mice. 3 key findings →

Evidence: low

Cognitive processes and their decline with aging were studied in individuals with Down Syndrome (DS) and individuals of comparable mental handicap without Down Syndrome (NonDS). 1 key finding →

Evidence: low

Nascent polypeptide-associated complex (NAC) protein, a heterodimeric complex of alpha- and beta-subunits, prevents mistargeting of nascent polypeptide chains to the endoplasmic reticulum membranes. alpha-NAC has sequence similarities with transcription-regulating proteins and has been reported to function as a transcriptional coactivator potentiating c-Jun-mediated transcription. 4 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