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Research

31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–25 of 43 studies in Disease mechanisms published 2026 · free to read (page 1 of 2) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 43 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; 16,851 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.

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

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

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

Comorbid neuropathologies but not Braak stage influence cognitive impairment in primary age-related tauopathy

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Journal of Neuropathology & Experimental Neurology 2026-05-02

Primary age-related tauopathy (PART) is a β-amyloid-independent tauopathy, thought by some to be a distinct process from Alzheimer disease neuropathologic change (ADNC). 3 key findings →

Design: longitudinal study Participants: 174 Evidence: moderate

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

Spatiotemporal transcriptomic profiling reveals upregulation of glycolysis pathway genes before overt tauopathy in the PS19 mouse model

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Experimental & Molecular Medicine 2026-02-13

The abnormal accumulation of hyperphosphorylated tau in neurofibrillary tangles is a hallmark of neurodegenerative diseases, such as Alzheimer's disease (AD) and frontotemporal dementia. 2 key findings →

Evidence: low

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

Classification of tauopathies from human brain homogenates through salt‐modulated tau amplification

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Alzheimer s & Dementia 2026-02-01

This method differentiated eight tauopathies, including Alzheimer's disease, Pick disease, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), argyrophilic grain disease (AGD), frontotemporal dementia with parkinsonism associated with chromosome 17 with N279K mutation (FTDP-17 N279K), and globular glial tauopathies types II and III. 5 key findings →

Evidence: low

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

Sex differences for clinical presentations and co-pathologies in four-repeat tauopathies

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Biology of Sex Differences 2026-04-03

Most common clinical diagnosis was PSP (41%) for PSP; unspecified FTD (36%) for CBD; AD for AGD (57%) and Other-4R groups (48%), without sex differences. 5 key findings →

Participants: 175 Evidence: low

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

Scalable human neuronal models of tauopathy producing endogenous seed-competent 4R tau

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Science Advances 2026-07-31

The accumulation of pathological four-repeat (4R) tau is central to several frontotemporal dementia (FTD) subtypes, but human neuronal models amenable to high-throughput screening of 4R tau-targeting therapies remain very limited. 1 key finding →

Evidence: low

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

Microglial Plasticity in Vascular Dementia: Mechanisms and Therapeutic Reprogramming

✓ Peer-reviewed alzhub usefulness score 39 out of 100. International Journal of Molecular Sciences 2026-04-22

Vascular dementia (VaD) is a leading cause of cognitive decline and arises from heterogeneous cerebrovascular pathologies, most commonly cerebral small vessel disease and chronic cerebral hypoperfusion. 1 key finding →

Evidence: low

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

Distinct regional patterns of synaptic vulnerability across hippocampal and parahippocampal subregions in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Brain Pathology 2026-02-09

Synaptic loss in the (para)hippocampus is a major contributor to cognitive decline in Alzheimer's disease (AD), yet its regional specificity and pathological correlates remain poorly understood. 5 key findings →

Evidence: low

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

Synaptic loss in alcohol use disorder: clinical and mechanistic insights from a PET imaging study

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Journal of Clinical Investigation 2026-03-31

Alcohol use disorder (AUD) is linked with changes in brain structure and function, with robust evidence for neurodegenerative changes, including synaptic loss in preclinical models. 2 key findings →

Evidence: low

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

Clinicopathological features of primary tauopathies: a brain bank series

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Frontiers in Neurology 2026-03-30

Fifteen cases were identified, spanning argyrophilic grain disease, primary age-related tauopathy, corticobasal degeneration, genetic frontotemporal dementia, and progressive supranuclear palsy. 5 key findings →

Evidence: low

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

Cinnamon Bud Extract Is a Source of Biomolecules Active against the Aggregation and Condensation of Alzheimer′s-Associated Tau Protein

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Journal of Agricultural and Food Chemistry 2026-04-02

High Resolution Image Download MS PowerPoint Slide Abnormal accumulation of tau fibrillar aggregates is a hallmark of tauopathies, including Alzheimer’s disease. 2 key findings →

Evidence: low

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

Overcoming the blood–brain barrier in Alzheimer's disease: translational perspectives on advanced drug delivery platforms

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Frontiers in Neuroscience 2026-05-14

Alzheimer's disease (AD) is the leading cause of dementia worldwide and represents a growing public health challenge in aging societies. 5 key findings →

Evidence: low

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

Gut Microbiome–Sphingolipid Metabolism–Brain Axis Interactions: Neuroprotective Effects of Amitriptyline as Functional Inhibitor of Acid Sphingomyelinase in a Mouse Model of Tauopathy

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Journal of Neuroimmune Pharmacology 2026-01-03

Tauopathies are neurodegenerative diseases characterized by accumulation of hyperphosphorylated tau protein (P-tau). 3 key findings →

Evidence: low

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

The In Vitro Multifaceted Biological Activity of Catechins in Relation to Their Oxidation Potentials

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Molecules 2026-04-17

In this study, the rank of multifaceted activity of catechin (C), epicatechin (EC), epigallocatechin (EGC), epicatechin-3-gallate (ECG) and epigallocatechin-3-gallate (EGCG) was addressed. 1 key finding →

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
  • Randomized / 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
  • Multicenter 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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.

1,048 records (3.3% of the library) are not peer-reviewed — 973 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