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Research

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

Find studies

Showing 8,901–8,925 of 10,985 studies · free to read (page 357 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.

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

Construction of human chromosome 21-specific yeast artificial chromosomes

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1989-12-01

Chromosome 21-specific yeast artificial chromosomes (YACs) have been constructed by a method that performs all steps in agarose, allowing size selection by pulsed-field gel electrophoresis and the use of nanogram to microgram quantities of DNA. 1 key finding →

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

Alzheimer-Like Pattern of Hypometabolism Emerges with Elevated Amyloid-β Burden in Down Syndrome

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of Alzheimer's disease : JAD 2018-01-01

In adults with DS, early amyloid-β accumulation in the striatum is divergent from sporadic AD; however, despite the early striatal amyloid-β, glucose hypometabolism was confined to the typical AD-associated regions, which occurs similarly in autosomal dominant AD. 1 key finding →

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

Poor Sleep as a Precursor to Cognitive Decline in Down Syndrome : A Hypothesis

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of Alzheimer's disease & Parkinsonism 2013-08-01

We propose that sleep disruption is a lever arm that influences how cognition emerges in development and then declines in response to Alzheimer disease in people with Down syndrome. 3 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

Regional selectivity of rab5 and rab7 protein upregulation in mild cognitive impairment and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of Alzheimer's disease : JAD 2010-01-01

Endocytic alterations are one of the earliest changes to occur in Alzheimer's disease (AD), and are hypothesized to be involved in the selective vulnerability of specific neuronal populations during the progression of AD. 2 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

Interactions between age, stress and insulin on cognition: implications for Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 2010-02-24

There is much interest in understanding the mechanisms responsible for interactions among stress, aging, memory and Alzheimer's disease. 4 key findings →

Evidence: low

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

The neurodegeneration mutant löchrig interferes with cholesterol homeostasis and Appl processing

✓ Peer-reviewed alzhub usefulness score 40 out of 100. The EMBO journal 2002-12-01

The novel Drosophila mutant löchrig (loe) shows progressive neurodegeneration and neuronal cell death, in addition to a low level of cholesterol ester. loe affects a specific isoform of the gamma-subunit of AMP-activated protein kinase (AMPK), a negative regulator of hydroxymethylglutaryl (HMG)-CoA reductase and cholesterol synthesis in vertebrates. 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

Developmental regulation of TREM2 and DAP12 expression in the murine CNS: implications for Nasu-Hakola disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neurochemical research 2008-04-11

Trem2 is an orphan, DAP12 associated receptor constitutively expressed in vivo by subsets of microglia in the healthy adult murine CNS and in vitro by subsets of oligodendrocytes in neonatal mixed glial cultures. 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