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Research

29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 3,301–3,325 of 8,227 studies · tagged Brain Biology (page 133 of 330) · 29,780 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.

Subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 15,255 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.

Nerve growth factor increases mRNA levels for the prion protein and the beta-amyloid protein precursor in developing hamster brain

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1988-12-01

Deposition of amyloid filaments serves as a pathologic hallmark for some neurodegenerative disorders. 1 key finding →

Evidence: low

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

Neurofibrillary tangles, granulovacuolar degeneration, and neuron loss in Down Syndrome: quantitative comparison with Alzheimer dementia

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Annals of neurology 1980-05-01

The degree of neurofibrillary tangle formation, granulovascuolar degeneration, and nerve cell loss was quantified in serial sections of the hippocampal formation from the brains of 5 adults dying with Down syndrome (monogolism). 1 key finding →

Evidence: low

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

Partial BACE1 reduction in a Down syndrome mouse model blocks Alzheimer-related endosomal anomalies and cholinergic neurodegeneration: role of APP-CTF

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neurobiology of aging 2015-12-02

β-amyloid precursor protein (APP) and amyloid beta peptide (Aβ) are strongly implicated in Alzheimer's disease (AD) pathogenesis, although recent evidence has linked APP-βCTF generated by BACE1 (β-APP cleaving enzyme 1) to the development of endocytic abnormalities and cholinergic neurodegeneration in early AD. 1 key finding →

Evidence: low

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

Link between DYRK1A overexpression and several-fold enhancement of neurofibrillary degeneration with 3-repeat tau protein in Down syndrome

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of neuropathology and experimental neurology 2011-01-01

Triplication of chromosome 21 in Down syndrome (DS) results in overexpression of the minibrain kinase/dual-specificity tyrosine phosphorylated and regulated kinase 1A gene (DYRK1A). 5 key findings →

Evidence: low

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

The physiological role of the amyloid precursor protein as an adhesion molecule in the developing nervous system

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of neurochemistry 2017-08-15

The amyloid precursor protein (APP) is a type I transmembrane glycoprotein better known for its participation in the physiopathology of Alzheimer disease as the source of the beta amyloid fragment. 5 key findings →

Evidence: low

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

Tau missorting and spastin-induced microtubule disruption in neurodegeneration: Alzheimer Disease and Hereditary Spastic Paraplegia

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Molecular neurodegeneration 2015-12-21

In Alzheimer Disease (AD), the mechanistic connection of the two major pathological hallmarks, namely deposition of Amyloid-beta (Aβ) in the form of extracellular plaques, and the pathological changes of the intracellular protein Tau (such as phosphorylation, missorting, aggregation), is not well understood. 2 key findings →

Evidence: low

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

Insulin resistance, oxidative stress and mitochondrial defects in Ts65dn mice brain: A harmful synergistic path in down syndrome

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Free radical biology & medicine 2021-01-29

Dysregulation of brain insulin signaling with reduced downstream neuronal survival and plasticity mechanisms are fundamental abnormalities observed in Alzheimer disease (AD). 4 key findings →

Evidence: low

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

N-truncated Aβ4-x peptides in sporadic Alzheimer's disease cases and transgenic Alzheimer mouse models

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Alzheimer's research & therapy 2017-10-04

The findings of this study are consistent with previous reports demonstrating a high aggregation propensity of Aβ 4-x peptides and suggest an important role of these N-truncated Aβ species in the process of amyloidogenesis and plaque core formation. 1 key finding →

Evidence: low

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

The BACH1/Nrf2 Axis in Brain in Down Syndrome and Transition to Alzheimer Disease-Like Neuropathology and Dementia

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Antioxidants (Basel, Switzerland) 2020-08-21

Down syndrome (DS) is the most common genetic cause of intellectual disability that is associated with an increased risk to develop early-onset Alzheimer-like dementia (AD). 3 key findings →

Evidence: low

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

APP mutations in the Aβ coding region are associated with abundant cerebral deposition of Aβ38

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Acta neuropathologica 2012-11-13

Aβ is the main component of amyloid deposits in Alzheimer disease (AD) and its aggregation into oligomers, protofibrils and fibrils is considered a seminal event in the pathogenesis of AD. 2 key findings →

Evidence: low

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

Parallel compensatory and pathological events associated with tau pathology in middle aged individuals with Down syndrome

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of neuropathology and experimental neurology 2003-09-01

Aged individuals with Down syndrome (DS) develop senile plaques and neurofibrillary tangles consistent with Alzheimer disease (AD). 1 key finding →

Participants: 15 Evidence: low

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

Down syndrome: age-dependence of PiB binding in postmortem frontal cortex across the lifespan

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neurobiology of aging 2017-03-14

Beta-amyloid (Aβ) deposition in brain accumulates as a function of age in people with Down syndrome (DS) with subsequent development into Alzheimer disease neuropathology, typically by 40 years of age. 3 key findings →

Participants: 25 Evidence: low

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

γ-Secretase Modulator BPN15606 Reduced Aβ42 and Aβ40 and Countered Alzheimer-Related Pathologies in a Mouse Model of Down Syndrome

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Annals of neurology 2024-05-15

Our findings point to the involvement of increased levels of Aβ42 and/or Aβ40 in contributing to several molecular and cognitive traits associated with DS-AD. 4 key findings →

Evidence: low

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

Proteome Signature of Alzheimer-Like Phenotypes in Frontal Cortices From Young and Old Individuals With Down Syndrome

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Molecular neurobiology 2025-11-21

Down syndrome (DS) stands out as the most prevalent genetic contributor to intellectual disability, marked by the presence of an extra copy of chromosome 21 (HSA21). 4 key findings →

Evidence: low

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

Alzheimer's disease: redox dysregulation as a common denominator for diverse pathogenic mechanisms

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Antioxidants & redox signaling 2012-02-07

Alzheimer's disease (AD) is the most common cause of dementia and a progressive neurodegeneration that appears to result from multiple pathogenic mechanisms (including protein misfolding/aggregation, involved in both amyloid β-dependent senile plaques and tau-dependent neurofibrillary tangles), metabolic and mitochondrial dysfunction, excitoxicity, calcium handling impairment, glial cell dysfunction, neuroinflammation, and oxidative stress. 3 key findings →

Evidence: low

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

Nuclear but not mitochondrial-encoded oxidative phosphorylation genes are altered in aging, mild cognitive impairment, and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2016-10-25

Our findings suggest that restoration of the expression of nuclear-encoded OXPHOS genes in aging could be a viable strategy for blunting AD progression. 4 key findings →

Evidence: low

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

Beta-amyloid-induced glial expression of both pro- and anti-inflammatory cytokines in cerebral cortex of aged transgenic Tg2576 mice with Alzheimer plaque pathology

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Brain research 2001-03-01

To elucidate the mechanisms involved in beta-amyloid-mediated inflammation in Alzheimer's disease, transgenic Tg2576 mice containing as transgene the Swedish double mutation of human amyloid precursor protein 695, were examined for the expression pattern of various cytokines using double immunocytochemistry and laser scanning microscopy. 4 key findings →

Evidence: low

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

Age-dependent neurodegeneration and Alzheimer-amyloid plaque formation in transgenic Drosophila

✓ Peer-reviewed alzhub usefulness score 43 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2004-04-01

Beta-amyloid peptides that are cleaved from the amyloid precursor protein (APP) play a critical role in Alzheimer's disease (AD) pathophysiology. 3 key findings →

Evidence: low

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

Lysosomal hydrolases of different classes are abnormally distributed in brains of patients with Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1991-12-01

beta-Amyloid formation requires multiple abnormal proteolytic cleavages of amyloid precursor protein (APP), including one within its intramembrane domain. 4 key findings →

Evidence: low

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

Statins promote the degradation of extracellular amyloid {beta}-peptide by microglia via stimulation of exosome-associated insulin-degrading enzyme (IDE) secretion

✓ Peer-reviewed alzhub usefulness score 43 out of 100. The Journal of biological chemistry 2010-09-28

Epidemiological studies indicate that intake of statins decrease the risk of developing Alzheimer disease. 4 key findings →

Evidence: low

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

From across this tag

10 of the 8,203 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.

↑ Change the filters

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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.

1,037 records (3.5% of the library) are not peer-reviewed — 964 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