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Research

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

Find studies

Showing 23,276–23,300 of 27,146 studies marked Peer-reviewed (page 932 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.

Subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

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.

The 129 codon polymorphism of the prion protein gene influences earlier cognitive performance in Down syndrome subjects

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Journal of neurology 2003-06-01

Recently, a frequent prion protein gene (PRNP) polymorphism consisting of a methionine (M) for valine (V) substitution at codon 129 has been associated with cognitive impairment in elderly individuals. 4 key findings →

Evidence: low

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

Proteomic signatures and aberrations of mouse embryonic stem cells containing a single human chromosome 21 in neuronal differentiation: an in vitro model of Down syndrome

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Neuroscience 2004-01-01

Neurodegeneration in fetal development of Down syndrome (DS) patients is proposed to result in apparent neuropathological abnormalities and to contribute to the phenotypic characteristics of mental retardation and premature development of Alzheimer disease. 1 key finding →

Evidence: low

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

Age, adaptive behavior, and Alzheimer disease in Down syndrome: cross-sectional and longitudinal analyses

✓ Peer-reviewed alzhub usefulness score 37 out of 100. American journal of mental retardation : AJMR 1994-09-01

Cross-sectional and longitudinal analyses were used to compare age-related changes in adaptive functioning in institutionalized adults with and without Down syndrome. 2 key findings →

Design: cross-sectional Evidence: moderate

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

Transcriptome and metabolome analysis of crGART, a novel cell model of de novo purine synthesis deficiency: Alterations in CD36 expression and activity

✓ Peer-reviewed alzhub usefulness score 37 out of 100. PloS one 2021-07-20

In humans, GART [phosphoribosylglycinamide formyltransferase (EC 2.1.2.2) / phosphoribosylglycinamide synthetase (EC 6.3.4.13) / phosphoribosylaminoimidazole synthetase (EC 6.3.3.1)] is a trifunctional protein which catalyzes the second, third, and fifth reactions of the ten step de novo purine synthesis (DNPS) pathway. 3 key findings →

Evidence: low

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

Aging-related increase in oxidative stress correlates with developmental pattern of beta-secretase activity and beta-amyloid plaque formation in transgenic Tg2576 mice with Alzheimer-like pathology

✓ Peer-reviewed alzhub usefulness score 37 out of 100. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience 2004-11-01

The molecular mechanisms of beta-amyloidogenesis in sporadic Alzheimer's disease are still poorly understood. 4 key findings →

Evidence: low

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

The aging brain. Changes in the neuronal insulin/insulin receptor signal transduction cascade trigger late-onset sporadic Alzheimer disease (SAD). A mini-review

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Journal of neural transmission (Vienna, Austria : 1996) 2002-07-01

Aging of the brain has been demonstrated to be the main risk factor for late-onset sporadic AD what is in contrast to early-onset familial AD in which mutations predominate the pathology. 4 key findings →

Evidence: low

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

Upregulation of BACE1 and beta-amyloid protein mediated by chronic cerebral hypoperfusion contributes to cognitive impairment and pathogenesis of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Neurochemical research 2009-01-04

Chronic cerebral hypoperfusion (CCH) increases the risk of Alzheimer disease (AD) through several biologically plausible pathways, but the relationship between CCH and the development of AD remains uncertain. 4 key findings →

Evidence: low

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

Immunohistochemical characterization of microglia in Nasu-Hakola disease brains

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Neuropathology : official journal of the Japanese Society of Neuropathology 2010-12-01

Nasu-Hakola disease (NHD) is a rare autosomal recessive disorder, characterized by progressive presenile dementia and formation of multifocal bone cysts, caused by genetic mutations of DNAX-activation protein 12 (DAP12) or triggering receptor expressed on myeloid cells 2 (TREM2). 4 key findings →

Evidence: low

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

TREM2 Attenuates Aβ1-42-Mediated Neuroinflammation in BV-2 Cells by Downregulating TLR Signaling

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Neurochemical research 2019-05-27

The pathogenesis of late-onset Alzheimer's disease (LOAD) mainly involves abnormal accumulation of extracellular β-amyloid (Aβ) and the consequent neurotoxic effects. 4 key findings →

Evidence: low

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

Decreased drebrin mRNA expression in Alzheimer disease: correlation with tau pathology

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Journal of neuroscience research 2008-08-01

To investigate the mRNA expression of the dendritic spine protein drebrin in Alzheimer's disease (AD), we performed post-mortem in situ hybridization studies in brain sections from 20 AD patients and 21 controls. 4 key findings →

Evidence: low

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

Total Tau and Phosphorylated Tau Protein Serum Levels in Patients with Schizophrenia Compared with Controls

✓ Peer-reviewed alzhub usefulness score 37 out of 100. The Psychiatric quarterly 2017-12-01

Tau protein is located in the axons of neurons and in Alzheimer Disease, is abnormally phosphorylated and aggregates into paired helical filaments (neurofibrillary tangles) reflecting the degree of neurofibrillary pathology and neurodegeneration. 4 key findings →

Participants: 42 Evidence: low

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

Tau proteins in the temporal and frontal cortices in patients with vascular dementia

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Journal of neuropathology and experimental neurology 2015-02-01

We previously reported that, in the brains of older patients with vascular dementia (VaD), there is a distinctive accumulation of detergent-extractable soluble amyloid-β, with a predominance of Aβ42 species. 4 key findings →

Evidence: low

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

Cerebrospinal Fluid Markers of Synaptic Injury and Functional Connectivity in Alzheimer Disease: Protocol for a Cross-Sectional Study

✓ Peer-reviewed alzhub usefulness score 37 out of 100. JMIR research protocols 2019-07-17

Synaptic loss is the best surrogate for cognitive decline in Alzheimer disease (AD) and is more closely associated with cognitive function than amyloid or tau pathologies. 4 key findings →

Design: cross-sectional Participants: 20 Evidence: low

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

Cerebral glucose metabolism in patients with frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Journal of nuclear medicine : official publication, Society of Nuclear Medicine 1998-11-01

Frontotemporal dementia (FTD) is a dementia syndrome characterized by peculiar behavioral changes arising from frontotemporal involvement and distinct from Alzheimer's disease (AD). 4 key findings →

Design: post-hoc analysis Evidence: low

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

Consequences of not recognizing delirium superimposed on dementia in hospitalized elderly individuals

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Journal of gerontological nursing 2000-01-01

The purpose of this study was to describe the recognition and management of delirium in hospitalized patients with and without dementia. 4 key findings →

Design: clinical trial Evidence: low

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

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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