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Research

27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 5,276–5,300 of 10,985 studies · free to read (page 212 of 440) · 27,380 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; 12,859 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.

Magnetic resonance imaging biomarkers for the early diagnosis of Alzheimer's disease: a machine learning approach

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Frontiers in neuroscience 2015-09-01

Determination of sensitive and specific markers of very early AD progression is intended to aid researchers and clinicians to develop new treatments and monitor their effectiveness, as well as to lessen the time and cost of clinical trials. 5 key findings →

Evidence: moderate

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

Diagnostic contribution and therapeutic perspectives of transcranial magnetic stimulation in dementia

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology 2021-07-20

Transcranial magnetic stimulation (TMS) is a powerful tool to probe in vivo brain circuits, as it allows to assess several cortical properties such asexcitability, plasticity and connectivity in humans. 1 key finding →

Evidence: low

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

Bile acid quantification of 20 plasma metabolites identifies lithocholic acid as a putative biomarker in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Metabolomics : Official journal of the Metabolomic Society 2017-11-17

Levels of lithocholic acid were significantly enhanced in plasma of AD patients (50 ± 6 nM, p = 0.004) compared to healthy controls (32 ± 3 nM). 3 key findings →

Participants: 20 Evidence: low

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

Integration and relative value of biomarkers for prediction of MCI to AD progression: spatial patterns of brain atrophy, cognitive scores, APOE genotype and CSF biomarkers

✓ Peer-reviewed alzhub usefulness score 50 out of 100. NeuroImage. Clinical 2013-11-28

This study evaluates the individual, as well as relative and joint value of indices obtained from magnetic resonance imaging (MRI) patterns of brain atrophy (quantified by the SPARE-AD index), cerebrospinal fluid (CSF) biomarkers, APOE genotype, and cognitive performance (ADAS-Cog) in progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) within a variable follow-up period up to 6 years, using data from the Alzheimer's Disease Neuroimaging Initiative-1 (ADNI-1). 4 key findings →

Evidence: low

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

Quantitative electroencephalogram utility in predicting conversion of mild cognitive impairment to dementia with Lewy bodies

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurobiology of aging 2014-07-15

Mild cognitive impairment (MCI) as a precursor of dementia with Lewy bodies (DLB) is the focus of recent research, trying to explore the early mechanisms and possible biomarkers of DLB. 5 key findings →

Participants: 20 Evidence: low

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

Relation between subcortical grey matter atrophy and conversion from mild cognitive impairment to Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Journal of neurology, neurosurgery, and psychiatry 2015-04-22

Analysis of variances, adjusted for sex and age, showed that all structures, except the globus pallidus, were smaller in AD than in controls. 3 key findings →

Participants: 773 Evidence: low

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

Precursor of amyloid protein in Alzheimer disease undergoes fast anterograde axonal transport

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1990-02-01

In the brains of aged humans and cases of Alzheimer disease, deposits of amyloid in senile plaques are located in proximity to nerve processes. 4 key findings →

Evidence: low

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

Generation of beta-amyloid in the secretory pathway in neuronal and nonneuronal cells

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1993-03-01

The cellular mechanism underlying the generation of beta-amyloid in Alzheimer disease and its relationship to the normal metabolism of the amyloid precursor protein are unknown. 4 key findings →

Evidence: low

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

The presenilin 2 mutation (N141I) linked to familial Alzheimer disease (Volga German families) increases the secretion of amyloid beta protein ending at the 42nd (or 43rd) residue

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-03-01

To gain insights into the significance of presenilins (PS) in the pathogenetic mechanisms of early-onset familial Alzheimer disease (FAD), we expressed cDNAs for wild-type PS2 and PS2 with the Volga German (N141I) mutation in cultured cells and then examined the metabolism of the transfected proteins and their effect on the C-terminal properties of secreted amyloid beta protein (A beta). 4 key findings →

Evidence: low

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

Estimation of the genetic contribution of presenilin-1 and -2 mutations in a population-based study of presenile Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Human molecular genetics 1998-01-01

Two closely related genes, the presenilins ( PS ), located at chromosomes 14q24.3 and 1q42.1, have been identified for autosomal dominant Alzheimer disease (AD) with onset age below 65 years (presenile AD). 4 key findings →

Evidence: low

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

Amyloid beta-protein is degraded by cellular angiotensin-converting enzyme (ACE) and elevated by an ACE inhibitor

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of biological chemistry 2005-09-09

Human genetic data have associated angiotensin-converting enzyme (ACE) with Alzheimer disease (AD), and purified ACE has been reported to cleave synthetic amyloid beta-protein (Abeta) in vitro. 4 key findings →

Evidence: low

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

Protein phosphorylation regulates secretion of Alzheimer beta/A4 amyloid precursor protein

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1992-04-01

Extracellular deposition of the beta/A4 amyloid peptide is a characteristic feature of the brain in patients with Alzheimer disease. beta/A4 amyloid is derived from the amyloid precursor protein (APP), an integral membrane protein that exists as three major isoforms (APP695, APP751, and APP770). 4 key findings →

Evidence: low

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

Tumor necrosis factor-α synthesis inhibitor 3,6'-dithiothalidomide attenuates markers of inflammation, Alzheimer pathology and behavioral deficits in animal models of neuroinflammation and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Journal of neuroinflammation 2012-05-29

Neuroinflammation is associated with virtually all major neurodegenerative disorders, including Alzheimer's disease (AD). 4 key findings →

Evidence: moderate

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

High striatal amyloid beta-peptide deposition across different autosomal Alzheimer disease mutation types

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Archives of neurology 2009-12-01

Mutations in the amyloid precursor protein (APP), presenilin 1 (PSEN1), and presenilin 2 (PSEN2) genes lead to increased Abeta levels before symptoms arise. 4 key findings →

Participants: 30 Evidence: moderate

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

Aβ-induced acceleration of Alzheimer-related τ-pathology spreading and its association with prion protein

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Acta neuropathologica 2019-08-14

Extracellular deposition of amyloid β-protein (Aβ) in amyloid plaques and intracellular accumulation of abnormally phosphorylated τ-protein (p-τ) in neurofibrillary tangles (NFTs) represent pathological hallmark lesions of Alzheimer's disease (AD). 4 key findings →

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.

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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.

1,032 records (3.8% 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