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Research

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

Find studies

Showing 1,001–1,025 of 1,380 studies in Disease mechanisms (page 41 of 56) · 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.

Other 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.

What “Disease mechanisms” covers

Disease mechanisms — Cell- and molecule-level research into what actually goes wrong in Alzheimer's and related diseases.

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.

Passive immunization with anti-Tau antibodies in two transgenic models: reduction of Tau pathology and delay of disease progression

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 2011-08-12

The microtubule-associated protein Tau plays a critical role in the pathogenesis of Alzheimer disease and several related disorders (tauopathies). 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Neurodegeneration and defective neurotransmission in a Caenorhabditis elegans model of tauopathy

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2003-07-18

Frontotemporal dementia with parkinsonism chromosome 17 type (FTDP-17) is caused by mutations in MAPT, the gene encoding tau. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Immunohistochemical quantification of the synapse-related protein synaptophysin in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuroscience letters 1989-08-01

Alzheimer disease (AD) as well as other dementing disorders are characterized by a continuous loss of neurons in cortical and subcortical areas and probably by an extensive synaptic loss. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Frontotemporal dementia and Parkinsonism linked to chromosome 17: a new group of tauopathies

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain pathology (Zurich, Switzerland) 1998-04-01

Frontotemporal dementia is a neurological disorder characterised by personality changes, deterioration of memory and executive functions as well as stereotypical behaviour. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Familial multiple system tauopathy with presenile dementia: a disease with abundant neuronal and glial tau filaments

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-04-01

Neurofibrillary lesions made of hyperphosphorylated microtubule-associated protein tau constitute not only one of the defining neuropathological features of Alzheimer disease but also are present in a number of other neurodegenerative diseases with dementia. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Inducible expression of Tau repeat domain in cell models of tauopathy: aggregation is toxic to cells but can be reversed by inhibitor drugs

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 2005-10-24

We generated several cell models of tauopathy in order to study the mechanisms of neurodegeneration in diseases involving abnormal changes of tau protein. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Methylthioninium chloride (methylene blue) induces autophagy and attenuates tauopathy in vitro and in vivo

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Autophagy 2012-04-01

More than 30 neurodegenerative diseases including Alzheimer disease (AD), frontotemporal lobe dementia (FTD), and some forms of Parkinson disease (PD) are characterized by the accumulation of an aggregated form of the microtubule-binding protein tau in neurites and as intracellular lesions called neurofibrillary tangles. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Acetylated Tau Obstructs KIBRA-Mediated Signaling in Synaptic Plasticity and Promotes Tauopathy-Related Memory Loss

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuron 2016-03-31

Tau toxicity has been implicated in the emergence of synaptic dysfunction in Alzheimer's disease (AD), but the mechanism by which tau alters synapse physiology and leads to cognitive decline is unclear. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Reduction of soluble Abeta and tau, but not soluble Abeta alone, ameliorates cognitive decline in transgenic mice with plaques and tangles

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 2006-10-20

Increasing evidence points to soluble assemblies of aggregating proteins as a major mediator of neuronal and synaptic dysfunction. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

The potential for beta-structure in the repeat domain of tau protein determines aggregation, synaptic decay, neuronal loss, and coassembly with endogenous Tau in inducible mouse models of tauopathy

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2008-01-01

We describe two new transgenic mouse lines for studying pathological changes of Tau protein related to Alzheimer's disease. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Proteins in human brain cortex are modified by oxidation, glycoxidation, and lipoxidation. Effects of Alzheimer disease and identification of lipoxidation targets

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 2005-03-29

Diverse oxidative pathways, such as direct oxidation of amino acids, glycoxidation, and lipoxidation could contribute to Alzheimer disease pathogenesis. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

7,8-dihydroxyflavone prevents synaptic loss and memory deficits in a mouse model of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 2013-09-11

Synaptic loss in the brain correlates well with disease severity in Alzheimer disease (AD). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

A zebrafish model of tauopathy allows in vivo imaging of neuronal cell death and drug evaluation

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of clinical investigation 2009-04-13

Our aging society is confronted with a dramatic increase of patients suffering from tauopathies, which include Alzheimer disease and certain frontotemporal dementias. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Argyrophilic grain disease is a sporadic 4-repeat tauopathy

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neuropathology and experimental neurology 2002-06-01

Argyrophilic grain disease (AGD) was first reported as an adult-onset dementia, but recent studies have emphasized personality change, emotional imbalance, and memory problems as clinical features of AGD. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Phenolic compounds prevent amyloid β-protein oligomerization and synaptic dysfunction by site-specific binding

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 2012-03-05

Cerebral deposition of amyloid β protein (Aβ) is an invariant feature of Alzheimer disease (AD), and epidemiological evidence suggests that moderate consumption of foods enriched with phenolic compounds reduce the incidence of AD. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

PKC ε activation prevents synaptic loss, Aβ elevation, and cognitive deficits in Alzheimer's disease transgenic mice

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2011-01-01

Among the pathologic hallmarks of Alzheimer's disease (AD) neurodegeneration, only synaptic loss in the brains of AD patients closely correlates with the degree of dementia in vivo. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

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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