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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 64 studies in Science (New York, N.Y.) (page 1 of 3) · 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.

Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Science (New York, N.Y.) 2006-10-01

Ubiquitin-positive, tau- and alpha-synuclein-negative inclusions are hallmarks of frontotemporal lobar degeneration with ubiquitin-positive inclusions and amyotrophic lateral sclerosis. 1 key finding →

Evidence: low

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

Restoring hippocampal glucose metabolism rescues cognition across Alzheimer's disease pathologies

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Science (New York, N.Y.) 2024-08-23

Impaired cerebral glucose metabolism is a pathologic feature of Alzheimer's disease (AD), with recent proteomic studies highlighting disrupted glial metabolism in AD. 4 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

Oxidative damage linked to neurodegeneration by selective alpha-synuclein nitration in synucleinopathy lesions

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Science (New York, N.Y.) 2000-11-01

Aggregated alpha-synuclein proteins form brain lesions that are hallmarks of neurodegenerative synucleinopathies, and oxidative stress has been implicated in the pathogenesis of some of these disorders. 4 key findings →

Evidence: low

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

The C9orf72 GGGGCC repeat is translated into aggregating dipeptide-repeat proteins in FTLD/ALS

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Science (New York, N.Y.) 2013-02-07

Expansion of a GGGGCC hexanucleotide repeat upstream of the C9orf72 coding region is the most common cause of familial frontotemporal lobar degeneration and amyotrophic lateral sclerosis (FTLD/ALS), but the pathomechanisms involved are unknown. 2 key findings →

Evidence: low

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

Mutation-specific functional impairments in distinct tau isoforms of hereditary FTDP-17

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Science (New York, N.Y.) 1998-12-01

Tau proteins aggregate as cytoplasmic inclusions in a number of neurodegenerative diseases, including Alzheimer's disease and hereditary frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). 1 key finding →

Participants: 17 Evidence: low

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

How neuroinflammation contributes to neurodegeneration

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Science (New York, N.Y.) 2016-08-01

Neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and frontotemporal lobar dementia are among the most pressing problems of developed societies with aging populations. 2 key findings →

Evidence: low

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

Amyloid beta protein gene: cDNA, mRNA distribution, and genetic linkage near the Alzheimer locus

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Science (New York, N.Y.) 1987-02-01

The amyloid beta protein has been identified as an important component of both cerebrovascular amyloid and amyloid plaques of Alzheimer's disease and Down syndrome. 1 key finding →

Evidence: low

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

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

Structural maturation of neural pathways in children and adolescents: in vivo study

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Science (New York, N.Y.) 1999-03-01

Structural maturation of fiber tracts in the human brain, including an increase in the diameter and myelination of axons, may play a role in cognitive development during childhood and adolescence. 2 key findings →

Evidence: low

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

C9orf72 is required for proper macrophage and microglial function in mice

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Science (New York, N.Y.) 2016-03-01

Expansions of a hexanucleotide repeat (GGGGCC) in the noncoding region of the C9orf72 gene are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. 2 key findings →

Evidence: low

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

S-nitrosylation of parkin regulates ubiquitination and compromises parkin's protective function

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Science (New York, N.Y.) 2004-04-22

Parkin is an E3 ubiquitin ligase involved in the ubiquitination of proteins that are important in the survival of dopamine neurons in Parkinson's disease (PD). 4 key findings →

Evidence: low

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

Ubiquitination of G3BP1 mediates stress granule disassembly in a context-specific manner

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Science (New York, N.Y.) 2021-06-01

Stress granules are dynamic, reversible condensates composed of RNA and protein that assemble in eukaryotic cells in response to a variety of stressors and are normally disassembled after stress is removed. 2 key findings →

Evidence: low

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

Release of Alzheimer amyloid precursor derivatives stimulated by activation of muscarinic acetylcholine receptors

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Science (New York, N.Y.) 1992-10-01

Altered processing of the amyloid precursor protein (APP) is a central event in the formation of amyloid deposits in the brains of individuals with Alzheimer's disease. 3 key findings →

Evidence: low

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

The brain in AIDS: central nervous system HIV-1 infection and AIDS dementia complex

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Science (New York, N.Y.) 1988-02-01

Infection with human immunodeficiency virus type 1 (HIV-1) is frequently complicated in its late stages by the AIDS dementia complex, a neurological syndrome characterized by abnormalities in cognition, motor performance, and behavior. 4 key findings →

Evidence: low

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

Participation of presenilin 2 in apoptosis: enhanced basal activity conferred by an Alzheimer mutation

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Science (New York, N.Y.) 1996-12-01

Overexpression of the familial Alzheimer's disease gene Presenilin 2 (PS2) in nerve growth factor-differentiated PC12 cells increased apoptosis induced by trophic factor withdrawal or beta-amyloid. 4 key findings →

Evidence: low

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

Intraneuronal aluminum accumulation in amyotrophic lateral sclerosis and Parkinsonism-dementia of Guam

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Science (New York, N.Y.) 1982-09-01

Scanning electron microscopy with energy-dispersive x-ray spectrometry was used to analyze the elemental content of neurofibrillary tangle (NFT)-bearing and NFT-free neurons within the Sommer's sector (H1 region) of the hippocampus in Guamanian Chamorros with amyotrophic lateral sclerosis and parkinsonism-dementia and in neurologically normal controls. 1 key finding →

Evidence: low

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

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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