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Research

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 876–900 of 1,385 studies (page 36 of 56) · 28,180 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)

Showing 1,385 studies tagged amyloid-beta — clear

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; 13,658 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.

Levels of amyloid-beta-42 and CSF pressure are directly related in patients with Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of neural transmission (Vienna, Austria : 1996) 2017-09-02

Experimental data suggest that the cerebrospinal fluid (CSF) dynamic is involved in the clearance of beta-amyloid, a key event in the pathogenesis of Alzheimer's disease (AD). 4 key findings →

Participants: 16 Evidence: low

Full summary, score breakdown and related studies → Original source

Combination of plasma tumor necrosis factor receptors signaling proteins, beta-amyloid and apolipoprotein E for the detection of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Neuroscience letters 2013-03-15

Activation of inflammatory processes has been observed within the brain as well as periphery of subjects with Alzheimer's disease (AD). 3 key findings →

Participants: 153 Evidence: low

Full summary, score breakdown and related studies → Original source

Glial heme oxygenase-1 expression in Alzheimer disease and mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Neurobiology of aging 2005-04-15

We determined whether oxidative stress is an early event in the pathogenesis of sporadic Alzheimer disease (AD), and correlated oxidative stress with neuropsychological functions and neurofibrillary pathology in AD and mild cognitive impairment (MCI). 3 key findings →

Evidence: low

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

Electroacupuncture ameliorates beta-amyloid pathology and cognitive impairment in Alzheimer disease via a novel mechanism involving activation of TFEB (transcription factor EB)

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Autophagy 2021-02-23

Alzheimer disease (AD) is the most prevalent neurodegenerative disorder leading to dementia in the elderly. 1 key finding →

Evidence: low

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

Glutamate Transporter GLT1 Expression in Alzheimer Disease and Dementia With Lewy Bodies

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Frontiers in aging neuroscience 2018-04-26

Glutamate transporter solute carrier family 1, member 2 (GLT1/EAAT2), a major modulator of glutamate homeostasis in astrocytes, is assessed in post-mortem human brain samples of frontal cortex area 8 in advanced stages of Alzheimer disease (AD) and terminal stages of dementia with Lewy bodies (DLB) in order to gain understanding of astrogliopathy in diseases manifested by dementia. 4 key findings →

Evidence: low

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

Comprehensive analysis of APOE and selected proximate markers for late-onset Alzheimer's disease: patterns of linkage disequilibrium and disease/marker association

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Genomics 2007-04-16

The epsilon(4) allele of APOE confers a two- to fourfold increased risk for late-onset Alzheimer's disease (LOAD), but LOAD pathology does not all fit neatly around APOE. 3 key findings →

Evidence: low

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

Both apolipoprotein E and A-I genes are present in a nonmammalian vertebrate and are highly expressed during embryonic development

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-08-01

Apolipoprotein E (apoE) is associated with several classes of plasma lipoproteins and mediates uptake of lipoproteins through its ability to interact with specific cell surface receptors. 4 key findings →

Evidence: low

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

Frequency of the apolipoprotein E epsilon 2 allele is diminished in sporadic Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Neuroscience letters 1994-07-01

Recent data have demonstrated genetic disequilibrium between inheritance of the apolipoprotein E (apoE) epsilon 4 allele and increased risk of Alzheimer disease. 2 key findings →

Evidence: low

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

Changes in cerebral blood volume and amyloid pathology in aged Alzheimer APP/PS1 mice on a docosahexaenoic acid (DHA) diet or cholesterol enriched Typical Western Diet (TWD)

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Neurobiology of disease 2007-06-18

High dietary cholesterol and low dietary docosahexaenoic acid (DHA) intake are risk factors for Alzheimer's disease (AD). 2 key findings →

Evidence: low

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

Clinicopathological features of familial Alzheimer's disease associated with the M139V mutation in the presenilin 1 gene. Pedigree but not mutation specific age at onset provides evidence for a further genetic factor

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Brain : a journal of neurology 1997-03-01

Sixteen affected individuals are described from two families with early onset autosomal dominant familial Alzheimer's disease. 3 key findings →

Evidence: low

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

Redox proteomics and amyloid β-peptide: insights into Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of neurochemistry 2018-11-27

Alzheimer disease (AD) is a progressive neurodegenerative disorder associated with aging and characterized pathologically by the presence of senile plaques, neurofibrillary tangles, and neurite and synapse loss. 2 key findings →

Evidence: low

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

Increased level of active GSK-3beta in Alzheimer's disease and accumulation in argyrophilic grains and in neurones at different stages of neurofibrillary degeneration

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Neuropathology and applied neurobiology 2007-02-01

The somatodendritic accumulation of hyperphosphorylated tau proteins is an early event preceding the appearance of neurofibrillary tangles (NFT) in Alzheimer's disease (AD) and might be necessary for their formation. 2 key findings →

Evidence: low

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

Decreased levels of PSD95 and two associated proteins and increased levels of BCl2 and caspase 3 in hippocampus from subjects with amnestic mild cognitive impairment: Insights into their potential roles for loss of synapses and memory, accumulation of Abeta, and neurodegeneration in a prodromal stage of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of neuroscience research 2010-02-01

Alzheimer's disease (AD) is the most common form of dementia and is pathologically characterized by senile plaques, neurofibrillary tangles, synaptic disruption and loss, and progressive neuronal deficits. 2 key findings →

Evidence: low

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

Oxidative stress in Alzheimer disease and mild cognitive impairment: evidence from human data provided by redox proteomics

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Archives of toxicology 2015-07-01

Alzheimer disease (AD) is a neurodegenerative disease with many known pathological features, yet there is still much debate into the exact cause and mechanisms for progression of this degenerative disorder. 5 key findings →

Evidence: low

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

IFN-γ and TNF-α are involved during Alzheimer disease progression and correlate with nitric oxide production: a study in Algerian patients

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 2014-05-15

Alzheimer's disease (AD) is a neurodegenerative disease leading to a progressive and irreversible loss of mental functions. 5 key findings →

Participants: 25 Evidence: low

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

Redox proteomic analysis of carbonylated brain proteins in mild cognitive impairment and early Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Antioxidants & redox signaling 2010-03-01

Previous studies indicated increased levels of protein oxidation in brain from subjects with Alzheimer's disease (AD), raising the question of whether oxidative damage is a late effect of neurodegeneration or precedes and contributes to the pathogenesis of AD. 1 key finding →

Evidence: low

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

Evidence for seeding of beta -amyloid by intracerebral infusion of Alzheimer brain extracts in beta -amyloid precursor protein-transgenic mice

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2000-05-01

Many neurodegenerative diseases are associated with the abnormal sequestration of disease-specific proteins in the brain, but the events that initiate this process remain unclear. 4 key findings →

Evidence: low

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

Age-related learning deficits in transgenic mice expressing the 751-amino acid isoform of human beta-amyloid precursor protein

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1995-06-01

The beta-amyloid precursor protein (beta-APP), from which the beta-A4 peptide is derived, is considered to be central to the pathogenesis of Alzheimer disease (AD). 4 key findings →

Evidence: low

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

Partial reduction of BACE1 has dramatic effects on Alzheimer plaque and synaptic pathology in APP Transgenic Mice

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2007-07-06

The aspartyl protease beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) initiates processing of amyloid precursor protein (APP) into amyloid beta (Abeta) peptide, the major component of Alzheimer disease (AD) plaques. 4 key findings →

Evidence: low

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

The Alzheimer amyloid precursor protein. Identification of a stable intermediate in the biosynthetic/degradative pathway

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 1990-03-01

The amyloid forming beta-peptide of Alzheimer's disease is synthesized as part of a larger integral membrane precursor protein (beta APP) of which three alternatively spliced versions of 695, 751, and 770 amino acids have been described. 4 key findings →

Evidence: low

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

From across this tag

9 of the 1,383 studies in this tag, 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 9. The same 9 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.

1,034 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