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Research

29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 7,326–7,350 of 16,388 studies scoring 30–49 out of 100 (page 294 of 656) · 29,380 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; 14,855 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.

Retromer Proteins Reduced in Down Syndrome and the Dp16 Model: Impact of APP Dose and Preclinical Studies of a γ-Secretase Modulator

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Annals of neurology 2023-04-29

Our studies point to increased APP gene dose as a compromising retromer function in DS and suggest a causal role for Aβ42 and Aβ40. 2 key findings →

Evidence: low

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

Absence of familial association between dementia of Alzheimer type and Down syndrome

✓ Peer-reviewed alzhub usefulness score 41 out of 100. American journal of medical genetics 1989-08-01

The aim of this study was to test whether there is an excess of dementia of Alzheimer type (DAT) cases in Down syndrome (DS) relatives. 1 key finding →

Design: case-control study Evidence: moderate

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

Common pathogenic mechanisms in the hippocampus across neurodegenerative dementias: Alzheimer's disease, Down syndrome, and Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 41 out of 100. NPJ dementia 2025-10-27

For these neurodegenerative dementias, we observed that the chronological age did not align with their biological age, which was determined based on hippocampal transcript levels (i.e., transcriptional age). 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Evaluation of plasma Abeta(40) and Abeta(42) as predictors of conversion to Alzheimer's disease in patients with mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neurobiology of aging 2008-05-19

Numerous studies have shown a marked decrease of beta-amyloid(42) (Abeta(42)) in the cerebrospinal fluid (CSF) of patients with incipient Alzheimer's disease (AD). 2 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source

Tau conformational changes correspond to impairments of episodic memory in mild cognitive impairment and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Experimental neurology 2002-10-01

A multitiered strategy was adopted to assess tau conformational changes within fibrillar lesions during the progression of Alzheimer's disease (AD). 3 key findings →

Evidence: low

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

Effectiveness of a cognitive rehabilitation program in mild dementia (MD) and mild cognitive impairment (MCI): a case control study

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Archives of gerontology and geriatrics 2007-01-01

Data support the evidence that neuropsychological rehabilitation is effective in Alzheimer disease (AD), to strengthen the pharmacological treatment to delay the progression of dementia. 1 key finding →

Evidence: low

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

Upregulation of select rab GTPases in cholinergic basal forebrain neurons in mild cognitive impairment and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of chemical neuroanatomy 2011-06-12

Endocytic system dysfunction is one of the earliest disturbances that occur in Alzheimer's disease (AD), and may underlie the selective vulnerability of cholinergic basal forebrain (CBF) neurons during the progression of dementia. 3 key findings →

Evidence: low

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

Metabolic syndrome, mild cognitive impairment and Alzheimer's disease--the emerging role of systemic low-grade inflammation and adiposity

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Brain research bulletin 2012-08-18

The past decade has shed new light on the etiology of Alzheimer's disease (AD), which is the consequence of interactions between numerous lesions. 1 key finding →

Evidence: low

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

Amyloid beta-peptide interactions with neuronal and glial cell plasma membrane: binding sites and implications for Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of peptide science : an official publication of the European Peptide Society 2004-05-01

The extracellular accumulation of amyloid-beta (Abeta) in neuritic plaques is one of the characteristic hallmarks of Alzheimer's disease (AD), a progressive dementing neurodegenerative disorder of the elderly. 4 key findings →

Evidence: low

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

Deferoxamine inhibits iron induced hippocampal tau phosphorylation in the Alzheimer transgenic mouse brain

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neurochemistry international 2012-12-20

Prior work has shown that iron interacts with hyperphosphorylated tau, which contributes to the formation of neurofibrillary tangles (NFTs) in Alzheimer's disease (AD), whereas iron chelator desferrioxamine (DFO) slows down the clinical progression of the cognitive decline associated with this disease. 4 key findings →

Evidence: low

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

Biological inorganic and bioinorganic chemistry of neurodegeneration based on prion and Alzheimer diseases

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Dalton transactions (Cambridge, England : 2003) 2004-05-11

A change of the prion protein conformation results in a class of neurodegenerative diseases called the transmissible spongiform encephalopathies (like mad cow and Creutzfeld-Jakob diseases). 4 key findings →

Evidence: low

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

Patients with Alzheimer disease have lower levels of serum anti-amyloid peptide antibodies than healthy elderly individuals

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Experimental gerontology 2002-07-01

Active immunization with the human amyloid peptide (Abeta42) or passive immunization with anti-Abeta42 antibodies protects mice that express a mutant human amyloid precursor protein (APP) transgene from cerebral amyloid deposits. 4 key findings →

Evidence: low

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

The roles of amyloid precursor protein (APP) in neurogenesis: Implications to pathogenesis and therapy of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Cell adhesion & migration 2011-07-01

The amyloid-beta (Aβ) peptide is the derivative of amyloid precursor protein (APP) generated through sequential proteolytic processing by β- and γ-secretases. 4 key findings →

Evidence: low

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

RAC1 inhibition targets amyloid precursor protein processing by gamma-secretase and decreases Abeta production in vitro and in vivo

✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of biological chemistry 2005-09-08

beta-Amyloid peptides (Abeta) that form the senile plaques of Alzheimer disease consist mainly of 40- and 42-amino acid (Abeta 40 and Abeta 42) peptides generated from the cleavage of the amyloid precursor protein (APP). 4 key findings →

Evidence: low

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

Retinal amyloid peptides and complement factor H in transgenic models of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neuroreport 2011-08-01

Murine transgenic models of Alzheimer's disease (Tg-AD) have been useful to analyze the contribution of β-amyloid precursor protein (βAPP), Aβ42 peptide deposition, and the proinflammatory mechanisms that characterize Alzheimer-type neuropathology. 4 key findings →

Evidence: low

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

Amyloid beta peptide potentiates cytokine secretion by interleukin-1 beta-activated human astrocytoma cells

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1995-11-01

Neurodegenerative processes in Alzheimer disease (AD) are thought to be driven in part by the deposition of amyloid beta (A beta), a 39- to 43-amino acid peptide product resulting from an alternative cleavage of amyloid precursor protein. 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. 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 29,380 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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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.

1,037 records (3.5% of the library) are not peer-reviewed — 964 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