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Research

30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1,126–1,150 of 1,334 studies in Disease mechanisms marked Peer-reviewed (page 46 of 54) · 30,980 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)

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; 16,452 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.

Helicobacter pylori filtrate induces Alzheimer-like tau hyperphosphorylation by activating glycogen synthase kinase-3β

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of Alzheimer's disease : JAD 2015-01-01

Abnormal hyperphosphorylation of microtubule-associated protein tau is involved in the pathogenesis of several neurodegenerative disorders including Alzheimer's disease (AD). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Evidence for physiological down-regulation of brain oxidative phosphorylation in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Experimental neurology 1996-11-01

In vivo imaging of patients with Alzheimer's disease using positron emission tomography (PET) demonstrates progressive reductions in brain glucose metabolism and blood flow in relation to dementia severity, more so in association than primary cortical regions. 5 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

Altered Intrinsic Pyramidal Neuron Properties and Pathway-Specific Synaptic Dysfunction Underlie Aberrant Hippocampal Network Function in a Mouse Model of Tauopathy

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2016-01-01

The formation and deposition of tau protein aggregates is proposed to contribute to cognitive impairments in dementia by disrupting neuronal function in brain regions, including the hippocampus. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Soluble tau species, not neurofibrillary aggregates, disrupt neural system integration in a tau transgenic model

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neuropathology and experimental neurology 2011-07-01

Neurofibrillary tangles are a feature of Alzheimer disease and other tauopathies, and although they are generally believed to be markers of neuronal pathology, there is little evidence evaluating whether tangles directly impact neuronal function. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Bax deletion prevents neuronal loss but not neurological symptoms in a transgenic model of inherited prion disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2004-12-23

Transgenic Tg(PG14) mice express a mutant prion protein containing 14 octapeptide repeats, whose human homologue is associated with an inherited prion dementia. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Biochemical staging of synucleinopathy and amyloid deposition in dementia with Lewy bodies

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neuropathology and experimental neurology 2006-03-01

The primary feature of dementia with Lewy bodies (DLB) is the aggregation of alpha-synuclein into characteristic lesions: Lewy bodies (LBs) and Lewy neurites. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Progressive neurodegeneration in C. elegans model of tauopathy

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neurobiology of disease 2005-11-01

Discovery of various mutations in the tau gene among frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) families suggests gain-of-toxic function of wild-type or mutant tau as the mechanism for extensive neuronal loss. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Alzheimer's disease-associated neurotoxic mechanisms and neuroprotective strategies

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Current drug targets. CNS and neurological disorders 2005-08-01

The characteristic hallmarks of Alzheimer's disease (AD), the most common form of dementia in the elderly, include senile plaques, mainly composed of beta-amyloid (Abeta) peptide, neurofibrillary tangles and selective synaptic and neuronal loss in brain regions involved in learning and memory. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Controlled cortical impact results in an extensive loss of dendritic spines that is not mediated by injury-induced amyloid-beta accumulation

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neurotrauma 2013-10-12

The clinical manifestations that occur after traumatic brain injury (TBI) include a wide range of cognitive, emotional, and behavioral deficits. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Posttranslational modifications of tau--role in human tauopathies and modeling in transgenic animals

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Current drug targets 2004-08-01

Alzheimer's disease (AD) is characterized histopathologically by beta-amyloid-containing plaques, neurofibrillary tangles (NFT), reduced synaptic density, and neuronal loss in selected brain areas. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Activated actin-depolymerizing factor/cofilin sequesters phosphorylated microtubule-associated protein during the assembly of alzheimer-like neuritic cytoskeletal striations

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2009-10-01

In Alzheimer's disease (AD), rod-like cofilin aggregates (cofilin-actin rods) and thread-like inclusions containing phosphorylated microtubule-associated protein (pMAP) tau form in the brain (neuropil threads), and the extent of their presence correlates with cognitive decline and disease progression. 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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.

1,040 records (3.4% of the library) are not peer-reviewed — 965 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    Where this research is being discussed: events