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Research

30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 7,501–7,525 of 16,956 studies scoring 30–49 out of 100 (page 301 of 679) · 30,180 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)

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; 15,654 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.

Oxidative stress and mitochondrial dysfunction in Down syndrome

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Advances in experimental medicine and biology 2012-01-01

Down syndrome (DS) or trisomy 21 is the genetic disease with highest prevalence displaying phenotypic features that both include neurologic deficiencies and a number of clinical outcomes. 5 key findings →

Evidence: low

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

Bach1 overexpression in Down syndrome correlates with the alteration of the HO-1/BVR-a system: insights for transition to Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Alzheimer's disease : JAD 2015-01-01

Bach1, among the genes encoded on chromosome 21, is a transcription repressor, which binds to antioxidant response elements of DNA thus inhibiting the transcription of specific genes involved in the cell stress response including heme oxygenase-1 (HO-1). 1 key finding →

Evidence: low

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

Possible compensatory events in adult Down syndrome brain prior to the development of Alzheimer disease neuropathology: targets for nonpharmacological intervention

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Alzheimer's disease : JAD 2007-03-01

Adults with Down syndrome (DS) develop Alzheimer disease (AD) pathology progressively with age but clinical signs of dementia are delayed by at least 10 years after the first signs of disease. 5 key findings →

Evidence: low

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

Alzheimer Abeta peptide induces chromosome mis-segregation and aneuploidy, including trisomy 21: requirement for tau and APP

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Molecular biology of the cell 2009-12-23

Both sporadic and familial Alzheimer's disease (AD) patients exhibit increased chromosome aneuploidy, particularly trisomy 21, in neurons and other cells. 2 key findings →

Evidence: low

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

Total numbers of neurons and glial cells in cortex and basal ganglia of aged brains with Down syndrome--a stereological study

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Cerebral cortex (New York, N.Y. : 1991) 2011-03-22

The total numbers of neurons and glial cells in the neocortex and basal ganglia in adults with Down syndrome (DS) were estimated with design-based stereological methods, providing quantitative data on brains affected by delayed development and accelerated aging. 1 key finding →

Evidence: low

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

Tau and alpha-synuclein inclusions in a case of familial frontotemporal dementia and progressive aphasia

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of neuropathology and experimental neurology 2005-03-01

Recent studies have shown that neurofibrillary tangles are frequently accompanied by alpha-synuclein inclusions in sporadic and familial Alzheimer disease, in Down syndrome, in progressive supranuclear palsy, and Parkinsonism dementia complex of Guam. 2 key findings →

Evidence: low

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

Alzheimer-related altered white matter microstructural integrity in Down syndrome: A model for sporadic AD?

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Alzheimer's & dementia (Amsterdam, Netherlands) 2020-11-07

Our findings suggest that quantification of WM changes in DS could provide a promising and clinically relevant biomarker for AD clinical onset and progression. 2 key findings →

Evidence: low

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

Research attitudes in families of individuals with Down syndrome: importance for clinical trials

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Alzheimer's research & therapy 2022-11-23

This is one of the first formal studies to evaluate research attitudes among relatives of individuals with DS and shows the feasibility of using this approach to answer important questions that will guide trialists developing treatments for AD in DS. 1 key finding →

Evidence: moderate

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

Association between presenilin-1 polymorphism and maternal meiosis II errors in Down syndrome

✓ Peer-reviewed alzhub usefulness score 41 out of 100. American journal of medical genetics 2000-08-01

Several lines of evidence suggest a shared genetic susceptibility to Down syndrome (DS) and Alzheimer disease (AD). 2 key findings →

Participants: 168 Evidence: low

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

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

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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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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 (3.4% 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