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Research

31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 2,151–2,175 of 2,660 studies · free to read · tagged Brain Biology (page 87 of 107) · 31,380 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; 16,851 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.

Bioenergetic mechanisms in astrocytes may contribute to amyloid plaque deposition and toxicity

✓ Peer-reviewed alzhub usefulness score 40 out of 100. The Journal of biological chemistry 2015-03-26

Alzheimer disease (AD) is characterized neuropathologically by synaptic disruption, neuronal loss, and deposition of amyloid β (Aβ) protein in brain structures that are critical for memory and cognition. 3 key findings →

Evidence: low

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

Multimodality imaging of Alzheimer disease and other neurodegenerative dementias

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of nuclear medicine : official publication, Society of Nuclear Medicine 2014-11-20

Neurodegenerative diseases, such as Alzheimer disease, result in cognitive decline and dementia and are a leading cause of mortality in the growing elderly population. 2 key findings →

Evidence: low

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

Astrocyte activation imaging with 11C-acetate and amyloid PET in mild cognitive impairment due to Alzheimer pathology

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Nuclear medicine communications 2021-11-01

MTL 11C-acetate SUVR was significantly elevated in MCI compared to cognitively normal participants (P = 0.03; Cohen d = 1.76). 4 key findings →

Design: cross-sectional Evidence: low

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

MicroRNA-193b is a regulator of amyloid precursor protein in the blood and cerebrospinal fluid derived exosomal microRNA-193b is a biomarker of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Molecular medicine reports 2014-08-12

Amyloid precursor protein (APP) has an important function in the generation of Alzheimer's disease (AD). 5 key findings →

Evidence: low

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

The evolution of A beta peptide burden in the APP23 transgenic mice: implications for A beta deposition in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Molecular medicine (Cambridge, Mass.) 2001-09-01

We suggest that the APP23 Tg mouse may develop an earlier blockage in A beta clearance than the Tg2576 mice, resulting in a more severe accumulation of A beta in the perivascular drainage pathways and in the brain. 4 key findings →

Evidence: low

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

The impact of inflammation on cognitive function in older adults: implications for healthcare practice and research

✓ Peer-reviewed alzhub usefulness score 40 out of 100. The Journal of neuroscience nursing : journal of the American Association of Neuroscience Nurses 2012-08-01

Accumulating evidence suggests that levels of inflammation, an immune response, increase with age throughout the body and the brain. 2 key findings →

Evidence: low

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

Quantification of modified amyloid beta peptides in Alzheimer disease and Down syndrome brains

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of neuropathology and experimental neurology 1998-11-01

To gain insights into the different forms of modified amyloid beta peptides (A beta) in the Alzheimer disease (AD) and Down syndrome (DS) brain, we used two-site ELISAs with antibodies specific for isomerized (i.e. A beta with L-isoaspartate at positions 1 and 7) and pyroglutamate-modified (i.e. A beta beginning with pyroglutamate at position 3) forms of A beta to quantitate the levels of these different A beta peptides in formic acid extracts of AD and DS frontal cortex. 1 key finding →

Evidence: low

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

Truncation and Activation of Dual Specificity Tyrosine Phosphorylation-regulated Kinase 1A by Calpain I: A MOLECULAR MECHANISM LINKED TO TAU PATHOLOGY IN ALZHEIMER DISEASE

✓ Peer-reviewed alzhub usefulness score 40 out of 100. The Journal of biological chemistry 2015-04-27

Hyperphosphorylation and dysregulation of exon 10 splicing of Tau are pivotally involved in pathogenesis of Alzheimer disease (AD) and/or other tauopathies. 2 key findings →

Evidence: low

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

Positron emission tomography and neuropathologic estimates of fibrillar amyloid-β in a patient with Down syndrome and Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Archives of neurology 2011-11-01

Florbetapir PET can be used to detect increased cerebral-to-cerebellar fibrillar Aβ burden in a Down syndrome patient with Alzheimer disease, even in the presence of frequent amyloid angiopathy and diffuse plaques in the cerebellum. 3 key findings →

Evidence: low

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

Chronic high levels of the RCAN1-1 protein may promote neurodegeneration and Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Free radical biology & medicine 2013-01-29

The RCAN1 gene encodes three different protein isoforms: RCAN1-4, RCAN1-1L, and RCAN1-1S. RCAN1-1L is the RCAN1 isoform predominantly expressed in human brains. 2 key findings →

Evidence: low

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

Beyond amyloid: Immune, cerebrovascular, and metabolic contributions to Alzheimer disease in people with Down syndrome

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neuron 2022-04-25

People with Down syndrome (DS) have increased risk of Alzheimer disease (AD), presumably conferred through genetic predispositions arising from trisomy 21. 2 key findings →

Evidence: low

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

Antioxidant strategies for Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. The Proceedings of the Nutrition Society 2002-05-01

Oxidative damage is present within the brains of patients with Alzheimer's disease (AD), and is observed within every class of biomolecule, including nucleic acids, proteins, lipids and carbohydrates. 5 key findings →

Evidence: low

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

apl-1, a Caenorhabditis elegans gene encoding a protein related to the human beta-amyloid protein precursor

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1993-12-01

The major component of senile plaques found in the brains of Alzheimer disease patients is the beta-amyloid peptide, which is derived from a larger amyloid precursor protein (APP). 4 key findings →

Evidence: low

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

Multi-target-directed coumarin derivatives: hAChE and BACE1 inhibitors as potential anti-Alzheimer compounds

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Bioorganic & medicinal chemistry letters 2007-10-04

The complex etiology of Alzheimer's disease (AD) prompts scientists to develop multifunctional compounds to combat causes and symptoms of such neurodegeneration. 2 key findings →

Evidence: low

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

Hyperhomocysteinemia increases beta-amyloid by enhancing expression of gamma-secretase and phosphorylation of amyloid precursor protein in rat brain

✓ Peer-reviewed alzhub usefulness score 40 out of 100. The American journal of pathology 2009-03-05

Hyperhomocysteinemia and beta-amyloid (Abeta) overproduction are critical etiological and pathological factors in Alzheimer disease, respectively; however, the intrinsic link between them is still missing. 4 key findings →

Evidence: low

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

Shifting paradigms: The central role of microglia in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neurobiology of disease 2020-06-12

Recent human genetic studies have challenged long standing hypotheses about the chain of events in Alzheimer's disease (AD), as the identification of genetic risk factors in microglial genes supports a causative role for microglia in the disease. 4 key findings →

Evidence: low

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

Downregulation of TREM2 expression exacerbates neuroinflammatory responses through TLR4-mediated MAPK signaling pathway in a transgenic mouse model of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Molecular immunology 2021-12-24

Activation of glial cells and neuroinflammation play an important role in the onset and development of Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

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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.

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
  • Randomized / 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
  • Multicenter 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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.

1,048 records (3.3% of the library) are not peer-reviewed — 973 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