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Research

30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 151–175 of 807 studies · free to read (page 7 of 33) · 30,980 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)

Showing 807 studies tagged transgenic — clear

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; 16,452 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.

TDP-43 is intrinsically aggregation-prone, and amyotrophic lateral sclerosis-linked mutations accelerate aggregation and increase toxicity

✓ Peer-reviewed alzhub usefulness score 53 out of 100. The Journal of biological chemistry 2009-05-22

Non-amyloid, ubiquitinated cytoplasmic inclusions containing TDP-43 and its C-terminal fragments are pathological hallmarks of amyotrophic lateral sclerosis (ALS), a fatal motor neuron disorder, and frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U). 5 key findings →

Evidence: low

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

Targeting RNA foci in iPSC-derived motor neurons from ALS patients with a C9ORF72 repeat expansion

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Science translational medicine 2013-10-01

Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative condition characterized by loss of motor neurons in the brain and spinal cord. 3 key findings →

Evidence: low

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

Disturbance of nuclear and cytoplasmic TAR DNA-binding protein (TDP-43) induces disease-like redistribution, sequestration, and aggregate formation

✓ Peer-reviewed alzhub usefulness score 53 out of 100. The Journal of biological chemistry 2008-02-27

TAR DNA-binding protein 43 (TDP-43) is the disease protein in frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U) and amyotrophic lateral sclerosis (ALS). 5 key findings →

Evidence: low

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

RNA Binding Antagonizes Neurotoxic Phase Transitions of TDP-43

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Neuron 2019-02-27

TDP-43 proteinopathy is a pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementia where cytoplasmic TDP-43 inclusions are observed within degenerating regions of patient postmortem tissue. 5 key findings →

Evidence: low

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

Sortilin-mediated endocytosis determines levels of the frontotemporal dementia protein, progranulin

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Neuron 2010-11-01

Video abstract The most common inherited form of Frontotemporal Lobar Degeneration (FTLD) known stems from Progranulin (GRN) mutation and exhibits TDP-43 plus ubiquitin aggregates. 5 key findings →

Evidence: low

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

Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2013-10-29

Expanded hexanucleotide repeats in the chromosome 9 open reading frame 72 (C9orf72) gene are the most common genetic cause of ALS and frontotemporal degeneration (FTD). 4 key findings →

Evidence: low

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

beta-amyloid peptides enhance alpha-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2001-09-25

Alzheimer's disease and Parkinson's disease are associated with the cerebral accumulation of beta-amyloid and alpha-synuclein, respectively. 1 key finding →

Evidence: low

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

Wild-type human TDP-43 expression causes TDP-43 phosphorylation, mitochondrial aggregation, motor deficits, and early mortality in transgenic mice

✓ Peer-reviewed alzhub usefulness score 53 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2010-08-01

Transactivation response DNA-binding protein 43 (TDP-43) is a principal component of ubiquitinated inclusions in frontotemporal lobar degeneration with ubiquitin-positive inclusions and in amyotrophic lateral sclerosis (ALS). 2 key findings →

Evidence: low

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

ALS-linked TDP-43 mutations produce aberrant RNA splicing and adult-onset motor neuron disease without aggregation or loss of nuclear TDP-43

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2013-02-04

Transactivating response region DNA binding protein (TDP-43) is the major protein component of ubiquitinated inclusions found in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) with ubiquitinated inclusions. 5 key findings →

Evidence: low

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

Poly(ADP-Ribose) Prevents Pathological Phase Separation of TDP-43 by Promoting Liquid Demixing and Stress Granule Localization

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Molecular cell 2018-08-09

In amyotrophic lateral sclerosis (ALS) and frontotemporal degeneration (FTD), cytoplasmic aggregates of hyperphosphorylated TDP-43 accumulate and colocalize with some stress granule components, but how pathological TDP-43 aggregation is nucleated remains unknown. 5 key findings →

Evidence: low

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

Loss of C9ORF72 impairs autophagy and synergizes with polyQ Ataxin-2 to induce motor neuron dysfunction and cell death

✓ Peer-reviewed alzhub usefulness score 53 out of 100. The EMBO journal 2016-04-21

An intronic expansion of GGGGCC repeats within the C9ORF72 gene is the most common genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia (ALS-FTD). 3 key findings →

Evidence: low

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

Progranulin mediates caspase-dependent cleavage of TAR DNA binding protein-43

✓ Peer-reviewed alzhub usefulness score 53 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2007-09-01

TAR DNA binding protein-43 (TDP-43) is the pathologic substrate of neuronal and glial inclusions in frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTDL-U) and in amyotrophic lateral sclerosis (ALS). 1 key finding →

Evidence: low

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

Human neural cell type-specific extracellular vesicle proteome defines disease-related molecules associated with activated astrocytes in Alzheimer's disease brain

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Journal of extracellular vesicles 2022-01-01

In neurodegenerative diseases, extracellular vesicles (EVs) transfer pathogenic molecules and are consequently involved in disease progression. 2 key findings →

Evidence: low

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

ATP13A2 deficiency disrupts lysosomal polyamine export

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Nature 2020-01-29

ATP13A2 (PARK9) is a late endolysosomal transporter that is genetically implicated in a spectrum of neurodegenerative disorders, including Kufor-Rakeb syndrome-a parkinsonism with dementia 1 -and early-onset Parkinson's disease 2 . 4 key findings →

Evidence: low

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

Microbiota fasting-related changes ameliorate cognitive decline in obesity and boost ex vivo microglial function through the gut-brain axis

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Gut 2025-05-07

Both the Keto and ADF groups demonstrated significant weight loss, but cognitive performance improved most notably in the ADF group, in association with reduced inflammation. 5 key findings →

Participants: 96 Evidence: high

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

Evidence for astrocytosis in prodromal Alzheimer disease provided by 11C-deuterium-L-deprenyl: a multitracer PET paradigm combining 11C-Pittsburgh compound B and 18F-FDG

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Journal of nuclear medicine : official publication, Society of Nuclear Medicine 2012-01-01

Increased (11)C-DED binding throughout the brain of the MCI (11)C-PIB+ patients potentially suggests that astrocytosis is an early phenomenon in AD development. 2 key findings →

Evidence: low

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

Plasma long-chain omega-3 fatty acids and atrophy of the medial temporal lobe

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Neurology 2012-08-01

The long-chain ω-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are potential candidates for interventions to delay Alzheimer disease (AD), but evidence from clinical studies is mixed. 1 key finding →

Participants: 281 Evidence: low

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

Hypoxia-inducible factor 1alpha (HIF-1alpha)-mediated hypoxia increases BACE1 expression and beta-amyloid generation

✓ Peer-reviewed alzhub usefulness score 52 out of 100. The Journal of biological chemistry 2007-02-15

The incidence of Alzheimer disease (AD) and vascular dementia is greatly increased following cerebral ischemia and stroke in which hypoxic conditions occur in affected brain areas. beta-Amyloid peptide (Abeta), which is derived from the beta-amyloid precursor protein (APP) by sequential proteolytic cleavages from beta-secretase (BACE1) and presenilin-1 (PS1)/gamma-secretase, is widely believed to trigger a cascade of pathological events culminating in AD and vascular dementia. 4 key findings →

Evidence: low

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

Exogenous alpha-synuclein fibrils seed the formation of Lewy body-like intracellular inclusions in cultured cells

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2009-11-05

Cytoplasmic inclusions containing alpha-synuclein (alpha-Syn) fibrils, referred to as Lewy bodies (LBs), are the signature neuropathological hallmarks of Parkinson's disease (PD). 1 key finding →

Evidence: low

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

Eukaryotic stress granules are cleared by autophagy and Cdc48/VCP function

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Cell 2013-06-01

Stress granules and P bodies are conserved cytoplasmic aggregates of nontranslating messenger ribonucleoprotein complexes (mRNPs) implicated in the regulation of mRNA translation and decay and are related to RNP granules in embryos, neurons, and pathological inclusions in some degenerative diseases. 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
  • 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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.

1,040 records (3.4% of the library) are not peer-reviewed — 965 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