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Research

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

Find studies

Showing 1,476–1,500 of 3,529 studies · tagged Genetics (page 60 of 142) · 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.

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.

The two faces of protein misfolding: gain- and loss-of-function in neurodegenerative diseases

✓ Peer-reviewed alzhub usefulness score 49 out of 100. The EMBO journal 2008-01-01

The etiologies of neurodegenerative diseases may be diverse; however, a common pathological denominator is the formation of aberrant protein conformers and the occurrence of pathognomonic proteinaceous deposits. 1 key finding →

Evidence: low

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

Relative abundance of Alzheimer A beta amyloid peptide variants in Alzheimer disease and normal aging

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1994-08-01

The Alzheimer A beta amyloid peptide (A beta) is the principal proteinaceous component of amyloid associated with Alzheimer disease (AD). 4 key findings →

Evidence: low

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

Translation of the alzheimer amyloid precursor protein mRNA is up-regulated by interleukin-1 through 5'-untranslated region sequences

✓ Peer-reviewed alzhub usefulness score 49 out of 100. The Journal of biological chemistry 1999-03-01

The amyloid precursor protein (APP) has been associated with Alzheimer's disease (AD) because APP is processed into the beta-peptide that accumulates in amyloid plaques, and APP gene mutations can cause early onset AD. 4 key findings →

Evidence: low

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

Reversal of Alzheimer's-like pathology and behavior in human APP transgenic mice by mutation of Asp664

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2006-04-25

The deficits characteristic of Alzheimer's disease (AD) are believed to result, at least in part, from the neurotoxic effects of beta-amyloid peptides, a set of 39-43 amino acid fragments derived proteolytically from beta-amyloid precursor protein (APP). 4 key findings →

Evidence: low

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

Age-related amyloid beta deposition in transgenic mice overexpressing both Alzheimer mutant presenilin 1 and amyloid beta precursor protein Swedish mutant is not associated with global neuronal loss

✓ Peer-reviewed alzhub usefulness score 49 out of 100. The American journal of pathology 2000-07-01

To analyze the relationship between the deposition of amyloid beta peptides (Abeta) and neuronal loss in transgenic models of Alzheimer's disease (AD), we examined the frontal neocortex (Fc) and CA1 portion of hippocampus (CA1) in PSAPP mice doubly expressing AD-associated mutant presenilin 1 (PS1) and Swedish-type mutant beta amyloid precursor protein (APPsw) by morphometry of Abeta burden and neuronal counts. 4 key findings →

Evidence: low

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

Curcumin inhibits LPS-induced neuroinflammation by promoting microglial M2 polarization via TREM2/ TLR4/ NF-κB pathways in BV2 cells

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Molecular immunology 2019-10-04

Microglia mediate multiple facets of neuroinflammation, which plays a double-edged role in various brain diseases via distinct microglial phenotypes (deleterious M1 and neuroprotective M2). 4 key findings →

Evidence: low

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

TREM2- and DAP12-dependent activation of PI3K requires DAP10 and is inhibited by SHIP1

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Science signaling 2010-05-18

The activation and fusion of macrophages and of osteoclasts require the adaptor molecule DNAX-activating protein of 12 kD (DAP12), which contains immunoreceptor tyrosine-based activation motifs (ITAMs). 4 key findings →

Evidence: low

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

A genome-wide gene-expression analysis and database in transgenic mice during development of amyloid or tau pathology

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Cell reports 2015-01-22

We provide microarray data comparing genome-wide differential expression and pathology throughout life in four lines of "amyloid" transgenic mice (mutant human APP, PSEN1, or APP/PSEN1) and "TAU" transgenic mice (mutant human MAPT gene). 4 key findings →

Evidence: low

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

Alzheimer's-associated PLCγ2 is a signaling node required for both TREM2 function and the inflammatory response in human microglia

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Nature neuroscience 2020-06-08

Human genetic data indicate that microglial dysfunction contributes to the pathology of Alzheimer's disease (AD), exemplified by the identification of coding variants in triggering receptor expressed on myeloid cells 2 (TREM2) and, more recently, in PLCG2, a phospholipase-encoding gene expressed in microglia. 4 key findings →

Evidence: low

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

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

The genetic causes of basal ganglia calcification, dementia, and bone cysts: DAP12 and TREM2

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Neurology 2005-05-01

Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL), or Nasu-Hakola disease, is a presenile dementia associated with loss of myelin, basal ganglia calcification, and bone cysts. 4 key findings →

Evidence: low

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

TREM2, microglia, and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Mechanisms of ageing and development 2021-01-28

Triggering receptor expressed on myeloid cells 2 (TREM2) has been suggested to play a crucial role in Alzheimer's disease (AD) pathogenesis, as revealed by genome-wide association studies (GWAS). 4 key findings →

Evidence: low

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

ADAM17 is the main sheddase for the generation of human triggering receptor expressed in myeloid cells (hTREM2) ectodomain and cleaves TREM2 after Histidine 157

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Neuroscience letters 2017-09-18

Triggering receptor expressed in myeloid cells (TREM2) is a member of the immunoglobulin superfamily and is expressed in macrophages, dendritic cells, microglia, and osteoclasts. 4 key findings →

Evidence: low

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

A locked immunometabolic switch underlies TREM2 R47H loss of function in human iPSC-derived microglia

✓ Peer-reviewed alzhub usefulness score 49 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2019-12-23

Loss-of-function genetic variants of triggering receptor expressed on myeloid cells 2 (TREM2) are linked with an enhanced risk of developing dementias. 4 key findings →

Evidence: low

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

TREM2 protects from atherosclerosis by limiting necrotic core formation

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Nature cardiovascular research 2024-03-12

Atherosclerosis is a chronic disease of the vascular wall driven by lipid accumulation and inflammation in the intimal layer of arteries, and its main complications, myocardial infarction and stroke, are the leading cause of mortality worldwide [1], [2]. 4 key findings →

Evidence: low

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

Genetic variability in response to amyloid beta deposition influences Alzheimer's disease risk

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Brain communications 2019-10-10

Genome-wide association studies of late-onset Alzheimer's disease risk have previously identified genes primarily expressed in microglia that form a transcriptional network. 4 key findings →

Evidence: low

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

From across this tag

10 of the 3,521 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 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