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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 33 studies in Disease mechanisms published 2011 (page 1 of 2) · 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.

A peculiar constellation of tau pathology defines a subset of dementia in the elderly

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Acta neuropathologica 2011-03-25

Sporadic tauopathies are characterized by differential cellular and topographical predominance of phospho-tau immunoreactivity and biochemical distinction of the tau protein. 5 key findings →

Design: longitudinal study Evidence: moderate

Full summary, score breakdown and related studies → Original source

Presence of reactive microglia and neuroinflammatory mediators in a case of frontotemporal dementia with P301S mutation

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neuro-degenerative diseases 2011-01-05

Our findings suggest that microglial activation and the production of proinflammatory mediators by phospho-tau-positive neurons and glial cells may differentially contribute to neuronal death and disease progression in neurodegenerative tauopathies. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Emerging histomorphologic phenotypes of chronic traumatic encephalopathy in American athletes

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neurosurgery 2011-07-01

The emerging histomorphologic features of our CTE cohort may specify histologic criteria for CTE diagnosis, may identify emerging histologic variants of CTE and may facilitate more objective surveillance and accurate identification of sentinel CTE cases. 1 key finding →

Evidence: moderate

Full summary, score breakdown and related studies → Original source

The frontotemporal dementia mutation R406W blocks tau's interaction with the membrane in an annexin A2-dependent manner

✓ Peer-reviewed alzhub usefulness score 40 out of 100. The Journal of cell biology 2011-02-01

Changes of the microtubule-associated protein tau are central in Alzheimer's disease (AD) and frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Spines, plasticity, and cognition in Alzheimer's model mice

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neural plasticity 2011-11-28

The pathological hallmarks of Alzheimer's disease (AD)--widespread synaptic and neuronal loss and the pathological accumulation of amyloid-beta peptide (Aβ) in senile plaques, as well as hyperphosphorylated tau in neurofibrillary tangles--have been known for many decades, but the links between AD pathology and dementia and effective therapeutic strategies remain elusive. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Tau oligomers impair memory and induce synaptic and mitochondrial dysfunction in wild-type mice

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Molecular neurodegeneration 2011-06-06

This study identifies tau oligomers as an acutely toxic tau species in vivo, and suggests that tau oligomers induce neurodegeneration by affecting mitochondrial and synaptic function, both of which are early hallmarks in AD and other tauopathies. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Exosome-associated tau is secreted in tauopathy models and is selectively phosphorylated in cerebrospinal fluid in early Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 2011-11-04

Recent demonstrations that the secretion, uptake, and interneuronal transfer of tau can be modulated by disease-associated tau modifications suggest that secretion may be an important element in tau-induced neurodegeneration. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Seeding of normal Tau by pathological Tau conformers drives pathogenesis of Alzheimer-like tangles

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 2011-03-03

Neurofibrillary tangles (NFTs) in Alzheimer disease and related tauopathies are composed of insoluble hyperphosphorylated Tau protein, but the mechanisms underlying the conversion of highly soluble Tau into insoluble NFTs remain elusive. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → 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

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

Amyloid β: linking synaptic plasticity failure to memory disruption in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neurochemistry 2011-11-28

Mounting evidence suggests that amyloid beta-induced impairments in synaptic plasticity that is accompanied by cognitive decline and dementia represent key pathogenic steps of Alzheimer's disease. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Molecular mechanisms linking diabetes mellitus and Alzheimer disease: beta-amyloid peptide, insulin signaling, and neuronal function

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Molecular bioSystems 2011-03-24

The incidence of Alzheimer disease (AD) and diabetes mellitus (DM) is increasing at an alarming rate and has become a major public health concern worldwide. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

CREB-activity and nmnat2 transcription are down-regulated prior to neurodegeneration, while NMNAT2 over-expression is neuroprotective, in a mouse model of human tauopathy

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Human molecular genetics 2011-10-25

Tauopathies, characterized by neurofibrillary tangles (NFTs) of phosphorylated tau proteins, are a group of neurodegenerative diseases, including frontotemporal dementia and both sporadic and familial Alzheimer's disease. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Hyperphosphorylated Tau in an α-synuclein-overexpressing transgenic model of Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The European journal of neuroscience 2011-04-01

Although clinically distinct diseases, tauopathies and synucleinopathies share a common genesis and mechanisms, leading to overlapping degenerative changes within neurons. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

NMNAT suppresses tau-induced neurodegeneration by promoting clearance of hyperphosphorylated tau oligomers in a Drosophila model of tauopathy

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Human molecular genetics 2011-09-30

Tauopathies, including Alzheimer's disease, are a group of neurodegenerative diseases characterized by abnormal tau hyperphosphorylation that leads to formation of neurofibrillary tangles. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Dysregulated phosphorylation of Ca(2+) /calmodulin-dependent protein kinase II-α in the hippocampus of subjects with mild cognitive impairment and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neurochemistry 2011-09-28

Alzheimer's disease (AD) is a progressive, neurodegenerative disorder and the most prevalent senile dementia. 4 key findings →

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