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Research

27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 9,776–9,800 of 10,985 studies · free to read (page 392 of 440) · 27,380 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; 12,859 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.

Astrocyte-apolipoprotein E associations in senile plaques in Alzheimer disease and vascular lesions: a regional immunohistochemical study

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neuropathology and experimental neurology 1997-04-01

While apolipoprotein E (ApoE) and beta-amyloid (A beta) co-localize in senile plaques in cortex and cerebellum in Alzheimer disease (AD), the A beta-positive, predominantly diffuse plaques in the striatum do not exhibit ApoE immunoreactivity regardless of disease duration. 2 key findings →

Evidence: low

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

Glial alterations in human prion diseases: A correlative study of astroglia, reactive microglia, protein deposition, and neuropathological lesions

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Medicine 2018-04-01

Proteinopathies such as Alzheimer, Parkinson, and Huntington diseases, where aberrant proteins spread throughout the brain during disease progression, may share a molecular basis and mechanisms of propagation. 3 key findings →

Evidence: low

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

Analysis of the hippocampal proteome in ME7 prion disease reveals a predominant astrocytic signature and highlights the brain-restricted production of clusterin in chronic neurodegeneration

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 2013-12-23

Prion diseases are characterized by accumulation of misfolded protein, gliosis, synaptic dysfunction, and ultimately neuronal loss. 2 key findings →

Evidence: low

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

Astrocytic estrogen receptors and impaired neurotrophic responses in a rat model of perimenopause

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Frontiers in aging neuroscience 2015-09-29

In a perimenopausal model of middle-aged rats, the astrocyte estrogen receptor-alpha (ERa): ER-beta (ERb) ratio increased with the onset of acyclicity (constant estrus, CE) in association with impaired neurotrophic responses to estradiol (E2). 1 key finding →

Evidence: low

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

Dementia in Parkinson's Disease Correlates with α-Synuclein Pathology but Not with Cortical Astrogliosis

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Parkinson's disease 2012-04-22

Dementia is a common feature in Parkinson's disease (PD) and is considered to be the result of limbic and cortical Lewy bodies and/or Alzheimer changes. 2 key findings →

Evidence: low

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

Supplementation with ribonucleotide-based ingredient (Ribodiet®) lessens oxidative stress, brain inflammation, and amyloid pathology in a murine model of Alzheimer

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 2021-04-10

Alzheimer's disease (AD) is the most common type of dementia worldwide, characterized by the deposition of neurofibrillary tangles and amyloid-β (Aβ) peptides in the brain. 1 key finding →

Evidence: low

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

Efficacy of language assessment in Alzheimer's disease: comparing in-person examination and telemedicine

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Clinical interventions in aging 2006-01-01

Telemedicine can improve access to speech and language evaluation services which is relevant to both dementia and other neurological diseases of the elderly. 4 key findings →

Evidence: low

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

Apolipoprotein A-I: insights from redox proteomics for its role in neurodegeneration

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proteomics. Clinical applications 2013-01-01

Proteomics has a wide range of applications, including determination of differences in the proteome in terms of expression and post-translational protein modifications. 5 key findings →

Evidence: low

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

Fluorescent light-induced chromatid breaks distinguish Alzheimer disease cells from normal cells in tissue culture

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1996-05-01

The neurodegeneration and amyloid deposition of sporadic Alzheimer disease (AD) also occur in familial AD and in all trisomy-21 Down syndrome (DS) patients, suggesting a common pathogenetic mechanism. 1 key finding →

Evidence: low

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

Detection of Alzheimer Disease Pathology in Patients Using Biochemical Biomarkers: Prospects and Challenges for Use in Clinical Practice

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The journal of applied laboratory medicine 2020-01-01

Thirty-four years ago, amyloid-β 1-42 peptide was identified in amyloid plaques from brain tissue obtained from patients with Alzheimer disease (AD) and Down syndrome. 5 key findings →

Evidence: low

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

Mitochondrial Imbalance in Down Syndrome: A Driver of Accelerated Brain Aging?

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Aging and disease 2025-04-06

Down syndrome (DS), caused by trisomy of chromosome 21 (HSA21), is a complex condition associated with neurodevelopmental impairments and accelerated brain aging, often culminating in early-onset Alzheimer's disease (AD). 1 key finding →

Evidence: low

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

Paving the Way for Therapy: The Second International Conference of the Trisomy 21 Research Society

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Molecular syndromology 2018-10-30

In the last decade, a number of important research advances in different fields have allowed Down syndrome (DS) research to flourish, creating a time of both unparalleled opportunity and considerable challenge. 1 key finding →

Evidence: low

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

Increases of SET level and translocation are correlated with tau hyperphosphorylation at ser202/thr205 in CA1 of Ts65Dn mice

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neurobiology of aging 2016-06-23

SET is a multifunctional protein, but when present in the cytoplasm, acts as a powerful inhibitor of phosphatase 2A. We previously observed that in CA1 of Down syndrome (DS) patients, the level of SET is increased, and SET is translocated to the cytoplasm and associated with the hyperphosphorylation of tau at ser202/thr205. 2 key findings →

Evidence: low

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

Expression of the phagocytosis-essential protein TREM2 is down-regulated by an aluminum-induced miRNA-34a in a murine microglial cell line

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of inorganic biochemistry 2013-05-29

One of the key classical pathological features of Alzheimer's disease (AD) is the progressive accumulation of amyloid beta (Aβ42) peptides and their coalescence into highly insoluble senile plaque cores. 4 key findings →

Evidence: low

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

The role of hippocampal tau protein phosphorylation in isoflurane-induced cognitive dysfunction in transgenic APP695 mice

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Anesthesia and analgesia 2014-08-01

Previous studies have shown that exposure to inhaled anesthetics can cause cognitive dysfunction, suggesting that general anesthesia might be a risk factor for the development of Alzheimer disease. 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
  • 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.

1,032 records (3.8% 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