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Research

29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–21 of 21 studies in EMBO Molecular Medicine · free to read · 29,780 in the whole library · How the 0–100 score works

Download bibliography of these 21 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; 15,255 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 amyloid hypothesis of Alzheimer's disease at 25 years

✓ Peer-reviewed alzhub usefulness score 61 out of 100. EMBO Molecular Medicine 2016-03-29

Despite continuing debate about the amyloid β-protein (or Aβ hypothesis, new lines of evidence from laboratories and clinics worldwide support the concept that an imbalance between production and clearance of Aβ42 and related Aβ peptides is a very early, often initiating factor in Alzheimer's disease (AD). 5 key findings →

Evidence: low

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

sTREM2 cerebrospinal fluid levels are a potential biomarker for microglia activity in early-stage Alzheimer's disease and associate with neuronal injury markers

✓ Peer-reviewed alzhub usefulness score 60 out of 100. EMBO molecular medicine 2016-05-02

TREM2 is an innate immune receptor expressed on the surface of microglia. 4 key findings →

Design: cross-sectional Evidence: low

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

Tau PET correlates with different Alzheimer's disease-related features compared to CSF and plasma p-tau biomarkers

✓ Peer-reviewed alzhub usefulness score 59 out of 100. EMBO molecular medicine 2021-07-13

PET, CSF and plasma biomarkers of tau pathology may be differentially associated with Alzheimer's disease (AD)-related demographic, cognitive, genetic and neuroimaging markers. 3 key findings →

Participants: 400 Evidence: low

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

sTREM2 is associated with amyloid-related p-tau increases and glucose hypermetabolism in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 57 out of 100. EMBO molecular medicine 2023-01-09

Microglial activation occurs early in Alzheimer's disease (AD) and previous studies reported both detrimental and protective effects of microglia on AD progression. 4 key findings →

Design: cross-sectional Participants: 70 Evidence: moderate

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

Novel tau biomarkers phosphorylated at T181, T217 or T231 rise in the initial stages of the preclinical Alzheimer's continuum when only subtle changes in Aβ pathology are detected

✓ Peer-reviewed alzhub usefulness score 55 out of 100. EMBO molecular medicine 2020-11-10

In Alzheimer's disease (AD), tau phosphorylation in the brain and its subsequent release into cerebrospinal fluid (CSF) and blood is a dynamic process that changes during disease evolution. 4 key findings →

Evidence: low

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

Enhancing protective microglial activities with a dual function TREM2 antibody to the stalk region

✓ Peer-reviewed alzhub usefulness score 54 out of 100. EMBO molecular medicine 2020-03-10

Triggering receptor expressed on myeloid cells 2 (TREM2) is essential for the transition of homeostatic microglia to a disease-associated microglial state. 4 key findings →

Evidence: low

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

An Alzheimer-associated TREM2 variant occurs at the ADAM cleavage site and affects shedding and phagocytic function

✓ Peer-reviewed alzhub usefulness score 53 out of 100. EMBO molecular medicine 2017-10-01

Sequence variations occurring in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2) support an essential function of microglia and innate immunity in the pathogenesis of Alzheimer's disease (AD) and other neurodegenerative disorders. 4 key findings →

Evidence: low

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

Novel Alzheimer risk genes determine the microglia response to amyloid-β but not to TAU pathology

✓ Peer-reviewed alzhub usefulness score 52 out of 100. EMBO molecular medicine 2020-01-17

Polygenic risk scores have identified that genetic variants without genome-wide significance still add to the genetic risk of developing Alzheimer's disease (AD). 2 key findings →

Evidence: low

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

Opposite microglial activation stages upon loss of PGRN or TREM2 result in reduced cerebral glucose metabolism

✓ Peer-reviewed alzhub usefulness score 51 out of 100. EMBO molecular medicine 2019-06-01

Microglia adopt numerous fates with homeostatic microglia (HM) and a microglial neurodegenerative phenotype (MGnD) representing two opposite ends. 4 key findings →

Evidence: low

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

TREM2 shedding by cleavage at the H157-S158 bond is accelerated for the Alzheimer's disease-associated H157Y variant

✓ Peer-reviewed alzhub usefulness score 50 out of 100. EMBO molecular medicine 2017-10-01

We have characterised the proteolytic cleavage events responsible for the shedding of triggering receptor expressed on myeloid cells 2 (TREM2) from primary cultures of human macrophages, murine microglia and TREM2-expressing human embryonic kidney (HEK293) cells. 4 key findings →

Evidence: low

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

High-affinity interactions and signal transduction between Aβ oligomers and TREM2

✓ Peer-reviewed alzhub usefulness score 50 out of 100. EMBO molecular medicine 2018-11-01

Rare coding variants in the triggering receptor expressed on myeloid cells 2 (TREM2) are associated with increased risk for Alzheimer's disease (AD), but how they confer this risk remains uncertain. 4 key findings →

Evidence: low

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

G-quadruplex-binding small molecules ameliorate C9orf72 FTD/ALS pathology in vitro and in vivo

✓ Peer-reviewed alzhub usefulness score 49 out of 100. EMBO molecular medicine 2018-01-01

Intronic GGGGCC repeat expansions in C9orf72 are the most common known cause of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS), which are characterised by degeneration of cortical and motor neurons, respectively. 2 key findings →

Evidence: low

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

CSF progranulin increases in the course of Alzheimer's disease and is associated with sTREM2, neurodegeneration and cognitive decline

✓ Peer-reviewed alzhub usefulness score 48 out of 100. EMBO molecular medicine 2018-12-01

Progranulin (PGRN) is predominantly expressed by microglia in the brain, and genetic and experimental evidence suggests a critical role in Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

A proteomic network approach across the ALS-FTD disease spectrum resolves clinical phenotypes and genetic vulnerability in human brain

✓ Peer-reviewed alzhub usefulness score 46 out of 100. EMBO molecular medicine 2018-01-01

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are neurodegenerative diseases with overlap in clinical presentation, neuropathology, and genetic underpinnings. 4 key findings →

Evidence: low

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

Prediction of continuous amyloid positron emission tomography with fluid measures of phosphorylated tau and β-amyloid

✓ Peer-reviewed alzhub usefulness score 46 out of 100. EMBO Molecular Medicine 2025-12-01

CSF Aβ42/Aβ40 contributed most to identify Aβ-positivity, while continuous Aβ-PET load within the positive range was best predicted by plasma P-tau217. 1 key finding →

Participants: 1,053 Evidence: low

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

TDP-43 pathology triggers neuroinflammation and cognitive impairment by inducing microglial necroptosis

✓ Peer-reviewed alzhub usefulness score 36 out of 100. EMBO Molecular Medicine 2026-03-10

Pathological TAR DNA-binding protein-43 (TDP-43) is a defining feature of several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and 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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.

1,037 records (3.5% 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