alzhub.org
Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Research

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 76–100 of 1,159 studies (page 4 of 47) · 28,180 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 1,159 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; 13,658 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.

Hippocampal T cell infiltration promotes neuroinflammation and cognitive decline in a mouse model of tauopathy

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Brain : a journal of neurology 2016-11-05

Alzheimer's disease is characterized by the combined presence of amyloid plaques and tau pathology, the latter being correlated with the progression of clinical symptoms. 4 key findings →

Evidence: low

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

Differential role of triggering receptors expressed on myeloid cells 2 R47H in 3 neurodegenerative diseases based on a systematic review and meta-analysis

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Medicine 2020-01-01

The AD set included 23,092 cases and 30,920 controls, the ALS set included 7391 cases and 12,442 controls, and the PD set included 8498 patients and 9161 controls. 3 key findings →

Design: meta-analysis Participants: 23,092 Evidence: high

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

The role of clusterin, complement receptor 1, and phosphatidylinositol binding clathrin assembly protein in Alzheimer disease risk and cerebrospinal fluid biomarker levels

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Archives of general psychiatry 2011-02-01

Furthermore, the CSF biomarker analyses provide a first insight into the potentially predominant pathogenetic mechanism(s) underlying the association between AD risk and PICALM. 1 key finding →

Design: case-control study Participants: 4,254 Evidence: moderate

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

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

Unconventional translation of C9ORF72 GGGGCC expansion generates insoluble polypeptides specific to c9FTD/ALS

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Neuron 2013-02-12

Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are devastating neurodegenerative disorders with clinical, genetic, and neuropathological overlap. 1 key finding →

Evidence: low

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

TDP-43 and FUS in amyotrophic lateral sclerosis and frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 57 out of 100. The Lancet. Neurology 2010-10-01

Abnormal intracellular protein aggregates comprise a key characteristic in most neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 5 key findings →

Evidence: low

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

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

RAN proteins and RNA foci from antisense transcripts in C9ORF72 ALS and frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2013-11-18

The finding that a GGGGCC (G4C2) hexanucleotide repeat expansion in the chromosome 9 ORF 72 (C9ORF72) gene is a common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) links ALS/FTD to a large group of unstable microsatellite diseases. 3 key findings →

Evidence: low

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

TDP-43 repression of nonconserved cryptic exons is compromised in ALS-FTD

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Science (New York, N.Y.) 2015-08-01

Cytoplasmic aggregation of TDP-43, accompanied by its nuclear clearance, is a key common pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementia (ALS-FTD). 2 key findings →

Evidence: low

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

Microglial activation states drive glucose uptake and FDG-PET alterations in neurodegenerative diseases

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Science translational medicine 2021-10-13

2-Deoxy-2-[ 18 F]fluoro-d-glucose positron emission tomography (FDG-PET) is widely used to study cerebral glucose metabolism. 4 key findings →

Participants: 12 Evidence: low

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

Truncated stathmin-2 is a marker of TDP-43 pathology in frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 57 out of 100. The Journal of clinical investigation 2020-11-01

No treatment for frontotemporal dementia (FTD), the second most common type of early-onset dementia, is available, but therapeutics are being investigated to target the 2 main proteins associated with FTD pathological subtypes: TDP-43 (FTLD-TDP) and tau (FTLD-tau). 4 key findings →

Evidence: moderate

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

α-synuclein toxicity in neurodegeneration: mechanism and therapeutic strategies

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Nature medicine 2017-02-01

Alterations in α-synuclein dosage lead to familial Parkinson's disease (PD), and its accumulation results in synucleinopathies that include PD, dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). 4 key findings →

Evidence: low

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

Impact of zervimesine on the neuroinflammatory biomarker GFAP and related proteomic molecular correlates in plasma of participants from a phase 2 clinical trial in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Alzheimer's research & therapy 2026-04-06

Collectively, plasma biomarker findings in the low p-tau217 subgroup were more robust than in the mITT population. 5 key findings →

Design: clinical trial Evidence: high

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

From across this tag

10 of the 1,155 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.

↑ 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.

1,034 records (3.7% 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