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Research

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

Find studies

Showing 1–18 of 18 studies with an author at Ionis Pharmaceuticals (United States) (US) · 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.

Tau-targeting antisense oligonucleotide MAPTRx in mild Alzheimer's disease: a phase 1b, randomized, placebo-controlled trial

✓ Peer-reviewed alzhub usefulness score 71 out of 100. Nature Medicine 2023-04-24

Tau plays a key role in Alzheimer's disease (AD) pathophysiology, and accumulating evidence suggests that lowering tau may reduce this pathology. 1 key finding →

Design: phase-1-trial Participants: 46 Evidence: early

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

Exploratory Tau Biomarker Results From a Multiple Ascending-Dose Study of BIIB080 in Alzheimer Disease: A Randomized Clinical Trial

✓ Peer-reviewed alzhub usefulness score 68 out of 100. JAMA neurology 2023-12-01

In this randomized clinical trial, BIIB080 reduced tau biomarkers, including CSF t-tau, CSF p-tau181, and tau PET, which is associated with cognitive decline, in participants with mild AD. 5 key findings →

Design: clinical trial Participants: 13 Evidence: high

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

Premature polyadenylation-mediated loss of stathmin-2 is a hallmark of TDP-43-dependent neurodegeneration

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Nature neuroscience 2019-01-14

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are associated with loss of nuclear transactive response DNA-binding protein 43 (TDP-43). 1 key finding →

Evidence: low

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

Therapeutic reduction of ataxin-2 extends lifespan and reduces pathology in TDP-43 mice

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Nature 2017-04-12

Amyotrophic lateral sclerosis (ALS) is a rapidly progressing neurodegenerative disease that is characterized by motor neuron loss and that leads to paralysis and death 2-5 years after disease onset. 5 key findings →

Evidence: low

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

Mechanism of STMN2 cryptic splice-polyadenylation and its correction for TDP-43 proteinopathies

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Science (New York, N.Y.) 2023-03-16

Loss of nuclear TDP-43 is a hallmark of neurodegeneration in TDP-43 proteinopathies, 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

Antisense oligonucleotide silencing of FUS expression as a therapeutic approach in amyotrophic lateral sclerosis

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Nature medicine 2022-01-24

Fused in sarcoma (FUS) is an RNA-binding protein that is genetically and pathologically associated with rare and aggressive forms of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 2 key findings →

Evidence: low

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

RNA toxicity from the ALS/FTD C9ORF72 expansion is mitigated by antisense intervention

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Neuron 2013-10-01

A hexanucleotide GGGGCC repeat expansion in the noncoding region of the C9ORF72 gene is the most common genetic abnormality in familial and sporadic amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 1 key finding →

Evidence: low

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

Divergent roles of ALS-linked proteins FUS/TLS and TDP-43 intersect in processing long pre-mRNAs

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Nature neuroscience 2012-09-30

FUS/TLS (fused in sarcoma/translocated in liposarcoma) and TDP-43 are integrally involved in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. 1 key finding →

Evidence: low

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

Stress Granule Assembly Disrupts Nucleocytoplasmic Transport

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Cell 2018-04-05

Defects in nucleocytoplasmic transport have been identified as a key pathogenic event in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) mediated by a GGGGCC hexanucleotide repeat expansion in C9ORF72, the most common genetic cause of ALS/FTD. 1 key finding →

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

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

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

C9orf72 poly(GR) aggregation induces TDP-43 proteinopathy

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Science translational medicine 2020-09-01

TAR DNA-binding protein 43 (TDP-43) inclusions are a pathological hallmark of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS), including cases caused by G 4 C 2 repeat expansions in the C9orf72 gene (c9FTD/ALS). 3 key findings →

Evidence: low

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

Acute Trem2 reduction triggers increased microglial phagocytosis, slowing amyloid deposition in mice

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2021-07-01

Heterozygous genetic variants within the TREM2 gene show a strong association with increased Alzheimer's disease (AD) risk. 4 key findings →

Evidence: low

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

Onset of Alzheimer disease in apolipoprotein ɛ4 carriers is earlier in butyrylcholinesterase K variant carriers

✓ Peer-reviewed alzhub usefulness score 42 out of 100. BMC neurology 2024-04-09

The authors sought to examine the impact of the K-variant of butyrylcholinesterase (BCHE-K) carrier status on age-at-diagnosis of Alzheimer disease (AD) in APOE4 carriers. 4 key findings →

Design: post-hoc analysis Participants: 33 Evidence: low

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

↑ Change the filters

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