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Research

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

Find studies

Showing 1–25 of 27 studies with an author at VIB-KU Leuven Center for Brain & Disease Research (BE) (page 1 of 2) · 27,380 in the whole library · How the 0–100 score works

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.

Other 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.

Prognosis for patients with amyotrophic lateral sclerosis: development and validation of a personalised prediction model

✓ Peer-reviewed alzhub usefulness score 63 out of 100. The Lancet. Neurology 2018-03-26

Eight candidate predictors entered the prediction model: bulbar versus non-bulbar onset (univariable hazard ratio [HR] 1·71, 95% CI 1·63-1·79), age at onset (1·03, 1·03-1·03), definite versus probable or possible ALS (1·47, 1·39-1·55), diagnostic delay (0·52, 0·51-0·53), forced vital capacity (HR 0·99, 0·99-0·99), progression rate (6·33, 5·92-6·76), frontotemporal dementia (1·34, 1·20-1·50), and presence of a C9orf72 repeat expansion (1·45, 1·31-1·61), all p Interpretation We have developed an externally validated model to predict survival without tracheostomy and non-invasive ventilation for more than 23 h per day in European patients with ALS. 1 key finding →

Participants: 1,936 Evidence: moderate

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

A C9orf72 promoter repeat expansion in a Flanders-Belgian cohort with disorders of the frontotemporal lobar degeneration-amyotrophic lateral sclerosis spectrum: a gene identification study

✓ Peer-reviewed alzhub usefulness score 61 out of 100. The Lancet. Neurology 2011-12-07

A locus on chromosome 9p21 has been associated with both disorders, and we aimed to identify the causal gene within this region. 3 key findings →

Participants: 305 Evidence: moderate

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

Xenografted human microglia display diverse transcriptomic states in response to Alzheimer's disease-related amyloid-β pathology

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Nature neuroscience 2024-03-27

Microglia are central players in Alzheimer's disease pathology but analyzing microglial states in human brain samples is challenging due to genetic diversity, postmortem delay and admixture of pathologies. 4 key findings →

Evidence: low

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

Gain of Toxicity from ALS/FTD-Linked Repeat Expansions in C9ORF72 Is Alleviated by Antisense Oligonucleotides Targeting GGGGCC-Containing RNAs

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Neuron 2016-04-21

Hexanucleotide expansions in C9ORF72 are the most frequent genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia. 5 key findings →

Evidence: low

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

TDP-43 proteinopathies: a new wave of neurodegenerative diseases

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Journal of neurology, neurosurgery, and psychiatry 2020-11-11

Inclusions of pathogenic deposits containing TAR DNA-binding protein 43 (TDP-43) are evident in the brain and spinal cord of patients that present across a spectrum of neurodegenerative diseases. 1 key finding →

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

The changing scene of amyotrophic lateral sclerosis

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Nature reviews. Neuroscience 2013-03-06

Several recent breakthroughs have provided notable insights into the pathogenesis of amyotrophic lateral sclerosis (ALS), with some even shifting our thinking about this neurodegenerative disease and raising the question as to whether this disorder is a proteinopathy, a ribonucleopathy or both. 1 key finding →

Evidence: low

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

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

Endo-lysosomal dysregulations and late-onset Alzheimer's disease: impact of genetic risk factors

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Molecular neurodegeneration 2019-06-03

Increasing evidence supports that cellular dysregulations in the degradative routes contribute to the initiation and progression of neurodegenerative diseases, including Alzheimer's disease. 4 key findings →

Evidence: low

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

Triad of TDP43 control in neurodegeneration: autoregulation, localization and aggregation

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Nature reviews. Neuroscience 2021-03-02

Cytoplasmic aggregation of TAR DNA-binding protein 43 (TDP43; also known as TARDBP or TDP-43) is a key pathological feature of several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 4 key findings →

Evidence: low

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

Astrocytes in Alzheimer's Disease: Pathological Significance and Molecular Pathways

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Cells 2021-03-04

Astrocytes perform a wide variety of essential functions defining normal operation of the nervous system and are active contributors to the pathogenesis of neurodegenerative disorders such as Alzheimer's among others. 4 key findings →

Evidence: low

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

Knock-in models related to Alzheimer's disease: synaptic transmission, plaques and the role of microglia

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Molecular neurodegeneration 2021-07-15

Microglia are active modulators of Alzheimer's disease but their role in relation to amyloid plaques and synaptic changes due to rising amyloid beta is unclear. 4 key findings →

Evidence: low

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

Human stem cell-derived monocytes and microglia-like cells reveal impaired amyloid plaque clearance upon heterozygous or homozygous loss of TREM2

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2018-11-12

Murine microglia expressing the Alzheimer's disease-linked TREM2 R47H mutation display variable decrease in phagocytosis, while impaired phagocytosis is reported following loss of TREM2. 4 key findings →

Evidence: low

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

Fine‐mapping of the TMEM106B locus reveals four haplotypes that are differentially associated with risk for neurodegeneration

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Alzheimer s & Dementia 2025-12-01

Analysis of the genotyping data revealed that the TMEM106B locus consists of four major haplotypes: HA/Ha (covering the coding region), and HB/Hb (covering the upstream regulatory region). 5 key findings →

Participants: 182 Evidence: low

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

Genomics link obesity and type 2 diabetes to Alzheimers disease to unveil novel biological insights

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-17

Body mass index (BMI), type 2 diabetes (T2D) and related cardiometabolic features associate with Alzheimers disease (AD) risk, yet shared mechanisms remain poorly understood. 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. 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 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