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Research

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

Find studies

Showing 726–750 of 1,385 studies (page 30 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.

Crucial role of calbindin-D28k in the pathogenesis of Alzheimer's disease mouse model

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Cell death and differentiation 2014-05-23

Calbindin-D28k (CB), one of the major calcium-binding and buffering proteins, has a critical role in preventing a neuronal death as well as maintaining calcium homeostasis. 4 key findings →

Evidence: low

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

De novo deleterious genetic variations target a biological network centered on Aβ peptide in early-onset Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Molecular psychiatry 2015-07-21

We hypothesized that de novo variants (DNV) might participate in the genetic determinism of sporadic early-onset Alzheimer disease (EOAD, onset before 65 years). 4 key findings →

Evidence: low

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

Glycoprotein NMB: a novel Alzheimer's disease associated marker expressed in a subset of activated microglia

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Acta neuropathologica communications 2018-10-19

Alzheimer's disease (AD) is an irreversible, devastating neurodegenerative brain disorder characterized by the loss of neurons and subsequent cognitive decline. 4 key findings →

Evidence: low

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

APOE genotype and sex affect microglial interactions with plaques in Alzheimer's disease mice

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Acta neuropathologica communications 2019-05-21

Microglia affect Alzheimer's disease (AD) pathogenesis in opposing manners, by protecting against amyloid accumulation in early phases of the disease and promoting neuropathology in advanced stages. 4 key findings →

Evidence: low

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

The Alzheimer's disease-associated protective Plcγ2-P522R variant promotes immune functions

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Molecular neurodegeneration 2020-09-11

Microglia-specific genetic variants are enriched in several neurodegenerative diseases, including Alzheimer's disease (AD), implicating a central role for alterations of the innate immune system in the disease etiology. 4 key findings →

Evidence: low

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

Multi-tissue neocortical transcriptome-wide association study implicates 8 genes across 6 genomic loci in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Genome medicine 2021-05-04

Alzheimer's disease (AD) is an incurable neurodegenerative disease currently affecting 1.75% of the US population, with projected growth to 3.46% by 2050. 4 key findings →

Evidence: low

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

Integrative Brain Transcriptome Analysis Links Complement Component 4 andHSPA2to theAPOEε2 Protective Effect in Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Molecular psychiatry 2020-11-24

Mechanisms underlying the protective effect of apolipoprotein E ( APOE ) ε2 against Alzheimer’s disease (AD) are not well understood. 4 key findings →

Participants: 982 Evidence: low

Full summary, score breakdown and related studies → Original source

Shifts in gut microbiota composition in an APP/PSS1 transgenic mouse model of Alzheimer's disease during lifespan

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Letters in applied microbiology 2018-04-16

Alzheimer's disease (AD) is the most common form of dementia and one of the major causes of disability and dependency in older people. 4 key findings →

Evidence: low

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

Exercise alters the immune profile in Tg2576 Alzheimer mice toward a response coincident with improved cognitive performance and decreased amyloid

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Journal of neuroinflammation 2008-04-09

Inflammation is associated with Abeta pathology in Alzheimer's disease (AD) and transgenic AD models. 4 key findings →

Participants: 29 Evidence: low

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

Specific domains of beta-amyloid from Alzheimer plaque elicit neuron killing in human microglia

✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 1996-10-01

Alzheimer's disease (AD) is found to have striking brain inflammation characterized by clusters of reactive microglia that surround senile plaques. 4 key findings →

Evidence: low

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

Activation of Toll-like receptor 2 on microglia promotes cell uptake of Alzheimer disease-associated amyloid beta peptide

✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of biological chemistry 2005-12-09

The human G-protein-coupled formyl peptide receptor-like 1 (FPRL1) and its mouse homologue mFPR2 mediate the chemotactic activity of a variety of polypeptides associated with inflammation and bacterial infection, including the 42-amino acid form of amyloid beta peptide (Abeta42), a pathogenic factor in Alzheimer disease. 4 key findings →

Evidence: low

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

Lysosomal proteomics reveals mechanisms of neuronal APOE4-associated lysosomal dysfunction

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Autophagy 2025-10-17

: Aβ-β-amyloid; AD-Alzheimer disease; APMS-affinity purification mass spectrometry; APOE-apolipoprotein E; APP-amyloid beta precursor protein; BafA1-bafilomycin A1; CMA-chaperone-mediated autophagy; COP-coatomer; ER-endoplasmic reticulum; ERAD-endoplasmic reticulum-associated degradation; ERGIC-endoplasmic reticulum-Golgi intermediate compartment; FCCP-carbonyl cyanide p-trifluoromethoxyphenylhydrazone; GABA-gamma-aminobutyric acid; GFP-green fluorescent protein; GPI-glycerophosphoinositol; GPN-glycyl-L-phenylalanine 2-naphthylamide; HA-hemagglutinin protein tag; iPSC-induced pluripotent stem cells; LAMP1-lysosomal associated membrane protein 1; LGALS3BP-galectin 3 binding protein; LysoIP-lysosomal immunoprecipitation; MAPT-microtubule associated protein tau; MR-CTSB-magic red cathepsin B; MS-mass spectrometry; NFT-neurofibrillary tangles; PCA-principal component analysis; PLA-proximity ligation assay; PSEN1-presenilin 1; PSEN2-presenilin 2; p-MAPT/Tau-phospho-MAPT/tau; ROS-reactive oxygen species; RT-qPCR-reverse transcriptase quantitative polymerase chain reaction; SEM-standard error of the mean; siRNA-short interfering RNA; SRCR-scavenger receptor cysteine-rich domain; TMED-transmembrane p24 trafficking protein; TMEM192-transmembrane protein 192. 1 key finding →

Evidence: low

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

In vivo changes in microglial activation and amyloid deposits in brain regions with hypometabolism in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. European journal of nuclear medicine and molecular imaging 2010-09-16

BPs of [(11)C](R)PK11195 and [(11)C]PIB were significantly higher in the parietotemporal regions of AD patients than in ten healthy controls. 3 key findings →

Design: clinical trial Evidence: low

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

Apolipoprotein E immunoreactivity in cerebral amyloid deposits and neurofibrillary tangles in Alzheimer's disease and kuru plaque amyloid in Creutzfeldt-Jakob disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Brain Research 1991-02-01

Researchers conducted immunohistochemical studies on lipid changes in Alzheimer's disease brains using an antibody to apolipoprotein E. They unexpectedly discovered that apo E immunoreactivity was associated with amyloid in senile plaques, cerebral vessels, and neurofibrillary tangles, as well as in kuru plaques in Creutzfeldt-Jakob disease. 3 key findings →

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

MicroRNA expression in extracellular vesicles as a novel blood-based biomarker for Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2023-04-18

Brain cell-derived small extracellular vesicles (sEVs) in blood offer unique cellular and molecular information related to the onset and progression of Alzheimer's disease (AD). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

From across this tag

10 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 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 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