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Research

27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1,201–1,225 of 1,381 studies in Disease mechanisms (page 49 of 56) · 27,780 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; 13,259 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.

Soluble Aβ oligomers inhibit long-term potentiation through a mechanism involving excessive activation of extrasynaptic NR2B-containing NMDA receptors

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2011-05-01

In Alzheimer's disease (AD), dementia severity correlates strongly with decreased synapse density in hippocampus and cortex. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Impaired mitochondrial biogenesis, defective axonal transport of mitochondria, abnormal mitochondrial dynamics and synaptic degeneration in a mouse model of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Human molecular genetics 2011-08-25

Increasing evidence suggests that the accumulation of amyloid beta (Aβ) in synapses and synaptic mitochondria causes synaptic mitochondrial failure and synaptic degeneration in Alzheimer's disease (AD). 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Molecular mechanisms of neurodegeneration in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Human molecular genetics 2010-04-22

Alzheimer's disease (AD) is characterized by cognitive impairment, progressive neurodegeneration and formation of amyloid-beta (Abeta)-containing plaques and neurofibrillary tangles composed of hyperphosphorylated tau. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Reduced dendritic spine density on cerebral cortical pyramidal neurons in schizophrenia

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neurology, neurosurgery, and psychiatry 1998-10-01

The results support the concept of there being a defect in the fine structure of dendrites of pyramidal neurons, involving loss of spines, in schizophrenia and may help to explain the loss of cortical volume without loss of neurons in this condition, although the effect of neuroleptic drugs cannot be ruled out. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Early phenotypic changes in transgenic mice that overexpress different mutants of amyloid precursor protein in brain

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 1999-03-01

Transgenic mice overexpressing different forms of amyloid precursor protein (APP), i.e. wild type or clinical mutants, displayed an essentially comparable early phenotype in terms of behavior, differential glutamatergic responses, deficits in maintenance of long term potentiation, and premature death. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Protection of synapses against Alzheimer's-linked toxins: insulin signaling prevents the pathogenic binding of Abeta oligomers

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2009-02-02

Synapse deterioration underlying severe memory loss in early Alzheimer's disease (AD) is thought to be caused by soluble amyloid beta (Abeta) oligomers. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Roles of amyloid precursor protein and its fragments in regulating neural activity, plasticity and memory

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Progress in neurobiology 2003-05-01

Indeed, it has been proposed that reductions in the level or activity of certain APP fragments, in addition to accumulation of Abeta, may play a critical role in the cognitive dysfunction associated with AD, particularly early in the course of the disease. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Invited review: Estrogens effects on the brain: multiple sites and molecular mechanisms

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of applied physiology (Bethesda, Md. : 1985) 2001-12-01

Besides their well-established actions on reproductive functions, estrogens exert a variety of actions on many regions of the nervous system that influence higher cognitive function, pain mechanisms, fine motor skills, mood, and susceptibility to seizures; they also appear to have neuroprotective actions in relation to stroke damage and Alzheimer's disease. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Amyloid beta oligomers induce impairment of neuronal insulin receptors

✓ Peer-reviewed alzhub usefulness score 36 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2007-08-24

Recent studies have indicated an association between Alzheimer's disease (AD) and central nervous system (CNS) insulin resistance. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Amyloid beta -peptide inhibition of the PKA/CREB pathway and long-term potentiation: reversibility by drugs that enhance cAMP signaling

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2002-09-20

Changes in hippocampal function seem critical for cognitive impairment in Alzheimer's disease (AD). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Amyloid oligomers: formation and toxicity of Abeta oligomers

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The FEBS journal 2010-02-09

Alzheimer's disease (AD) is an age-related, progressive degenerative disorder that is characterized by synapse and neuron loss in the brain and the accumulation of protein-containing deposits (referred to as 'senile plaques') and neurofibrillary tangles. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Beta-amyloid activates the mitogen-activated protein kinase cascade via hippocampal alpha7 nicotinic acetylcholine receptors: In vitro and in vivo mechanisms related to Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2001-06-01

Alzheimer's Disease (AD) is the most common of the senile dementias, the prevalence of which is increasing rapidly, with a projected 14 million affected worldwide by 2025. 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.

1,034 records (3.7% 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