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Research

30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 26–50 of 184 studies in Disease mechanisms · free to read (page 2 of 8) · 30,580 in the whole library · How the 0–100 score works

Download bibliography of these 184 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.

Other subjects

Authors

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

Institutions

From OpenAlex; 16,054 studies have no institution on record and are not counted here.

What “Disease mechanisms” covers

Disease mechanisms — Cell- and molecule-level research into what actually goes wrong in Alzheimer's and related diseases.

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 single moderate to severe traumatic brain injury and long-term tauopathy in humans and preclinical animal models: a systematic narrative review of the literature

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Acta neuropathologica communications 2022-01-31

Of 4,150 studies screened, 26 were eligible for inclusion, of which 17 were human studies, 8 were preclinical animal studies, and 1 included both human and preclinical animal studies. 4 key findings →

Design: narrative review Participants: 12 Evidence: low

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

Insulin-degrading enzyme regulates the levels of insulin, amyloid β-protein, and the β-amyloid precursor protein intracellular domain in vivo

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Proceedings of the National Academy of Sciences 2003-03-12

Two substrates of insulin-degrading enzyme (IDE), amyloid beta-protein (Abeta) and insulin, are critically important in the pathogenesis of Alzheimer's disease (AD) and type 2 diabetes mellitus (DM2), respectively.

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

In Vivo Cortical Microstructure: Relationships With Tauopathy and Cognitive Impairment in the Elderly

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Journal of Neurochemistry 2025-08-01

Our results suggest that microstructural features derived from NODDI such as fISO might be useful adjunct markers to tau, which needs to be confirmed in longitudinal studies. 2 key findings →

Design: longitudinal study Participants: 80 Evidence: moderate

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

Charting the research frontier for viral infections, immunomodulation, and dementia: a perspective on synaptic biomarkers as essential clinical trial endpoints

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Frontiers in Cellular and Infection Microbiology 2026-01-05

The viral-inflammatory hypothesis of Alzheimer's disease offers a new paradigm, yet interventions like antivirals and vaccination present a paradox that challenge therapeutic development. 1 key finding →

Design: randomized controlled trial Evidence: high

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

Current advances and unmet needs in Alzheimer's disease trials for individuals with Down syndrome: Navigating new therapeutic frontiers

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Alzheimer s & Dementia 2025-06-01

Individuals with Down syndrome (DS) have a genetically determined form of Alzheimer's disease (AD) due to the amyloid precursor protein (APP) gene dose effect. 1 key finding →

Design: longitudinal study Evidence: moderate

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

What is cognitive reserve? Theory and research application of the reserve concept

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Journal of the International Neuropsychological Society 2002-03-01

The idea of reserve against brain damage stems from the repeated observation that there does not appear to be a direct relationship between the degree of brain pathology or brain damage and the clinical manifestation of that damage.

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

Abnormal phosphorylation of the microtubule-associated protein tau (tau) in Alzheimer cytoskeletal pathology.

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Proceedings of the National Academy of Sciences 1986-07-01

A monoclonal antibody to the microtubule-associated protein tau (tau) labeled some neurofibrillary tangles and plaque neurites, the two major locations of paired-helical filaments (PHF), in Alzheimer disease brain.

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

High-Level Neuronal Expression of Aβ1–42in Wild-Type Human Amyloid Protein Precursor Transgenic Mice: Synaptotoxicity without Plaque Formation

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Journal of Neuroscience 2000-06-01

Amyloid plaques are a neuropathological hallmark of Alzheimer's disease (AD), but their relationship to neurodegeneration and dementia remains controversial.

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

Synaptic markers are associated with cognitive decline after accounting for amyloid burden among an at-risk Alzheimer’s disease cohort

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Scientific Reports 2025-06-03

Amyloid burden impacts cognitive decline in the pre-dementia stages of Alzheimer's disease (AD), but there remains significant variability in cognitive trajectories that may be explainable by markers of synaptic function and neurodegeneration. 2 key findings →

Design: longitudinal study Evidence: moderate

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

Fluid Biomarkers of Cognitive Impairments Following Traumatic Brain Injury: A Systematic Review and Meta Analysis

✓ Peer-reviewed alzhub usefulness score 53 out of 100. International journal of molecular sciences 2026-05-11

Traumatic brain injury (TBI), a major cause of persistent cognitive impairment (CI), increases the long-term risk of developing dementia, including Alzheimer's disease (AD). 3 key findings →

Design: longitudinal study Participants: 29 Evidence: moderate

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

Investigating neuropathological correlates of hyperactive and psychotic symptoms in dementia: a systematic review

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Frontiers in dementia 2025-01-29

This systematic review aims to elucidate the neuropathological basis of the HIDA and psychosis domains, exploring whether distinct proteinopathies and neural circuit dysfunctions are associated with these symptoms. 4 key findings →

Design: systematic review Evidence: high

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

The Effects of Dietary Intervention and Macrophage-Activating Factor Supplementation on Cognitive Function in Elderly Users of Outpatient Rehabilitation

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Nutrients 2024-06-28

MAF supplementation improved cognitive function, especially after 6 months, in elderly people undergoing rehabilitation. 4 key findings →

Design: randomized controlled trial Evidence: low

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

Advanced Glycation End-Products Are Associated With the Presence and Severity of Paratonia in Early Stage Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Journal of the American Medical Directors Association 2017-05-27

From the 144 participants (56.3% female and 43.7% male, with a mean [standard deviation] age of 80.7 [7.7] years), 118 participants were available for final follow-up. 4 key findings →

Design: cohort study Participants: 144 Evidence: moderate

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

Single-cell atlas of transcriptomic vulnerability across brain disorders

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Nature 2026-09-23

. Here, to gain deeper insights into the aetiology of different brain diseases, we used specimens from 1,494 unique donors to generate a population-scale single-cell transcriptomic atlas of the human dorsolateral prefrontal cortex, comprising over 6.3 million individual nuclei. 1 key finding →

Evidence: moderate

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

Comprehensive metabolomics profiling reveals novel biomarkers and pathways for early detection of Alzheimer’s disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Brain Communications 2025-01-01

Clinical Dementia Rating-Global scores (1.44 ± 0.65 versus 0.24 ± 0.25; P < 0.0001) and Patient Health Questionnaire-9 scores (4.88 ± 4.21 versus 0.20 ± 0.50; P < 0.0001) were higher than controls. 4 key findings →

Design: cross-sectional Participants: 25 Evidence: moderate

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

Slowly progressive dementia caused by MAPT R406W mutations: longitudinal report on a new kindred and systematic review

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Alzheimer's research & therapy 2018-01-09

Dominance of 4R over three-repeat (exon 10-) tau isoforms contrasts with earlier reports of R406W patients and was not sufficiently explained by the presence of H1/H2 haplotypes in two of the autopsied patients. 3 key findings →

Design: systematic review 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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.

1,037 records (3.4% of the library) are not peer-reviewed — 964 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    Where this research is being discussed: events