alzhub.org
Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Research

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

Find studies

Showing 10,801–10,825 of 10,985 studies · free to read (page 433 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.

Diagnostic performance of plasma Aβ 1-42 , Aβ 1-40 and pTau 181 in the LUMIPULSE automated platform for the detection of Alzheimer disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2023-04-26

Recently-developed blood markers for Alzheimer’s (AD) detection have high accuracy but usually require ultra-sensitive analytic tools not commonly available in clinical laboratories. 4 key findings →

Participants: 136 Evidence: moderate

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

Down syndrome postmortem brains exhibit reduction in [ 18 F]nifene binding to α4β2* nicotinic acetylcholinergic receptors

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-15

Alzheimer’s disease (AD) pathology including amyloid beta (Aβ) plaques and tau tangles accumulate with age in Down Syndrome (DS). 4 key findings →

Evidence: low

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

Oligodendrocyte Enriched Brain Organoids Reveal Impaired Oligodendroglial Maturation and Altered Neural Network Activity in Down Syndrome

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-08-28

Individuals with Down syndrome (DS) display developmental delay, intellectual disability, premature brain ageing, and an increased risk of Alzheimer-like neurodegeneration. 4 key findings →

Evidence: low

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

Multi-dimensional attention framework for personalised Alzheimer's disease progression prediction across sporadic and genetic risk cohorts

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-08-03

Alzheimer's disease progresses heterogeneously across diverse cohorts, yet current predictive models fail to capture this complexity while remaining clinically interpretable. 4 key findings →

Design: longitudinal study Participants: 1,669 Evidence: moderate

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

Multi-dimensional attention framework for personalized Alzheimer’s disease progression prediction across sporadic and genetic risk cohorts

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2025-12-17

Alzheimer’s disease manifests through heterogeneous progression patterns across diverse populations, yet current predictive models fail to capture this complexity while maintaining clinical interpretability. 4 key findings →

Design: longitudinal study Participants: 1,669 Evidence: moderate

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

A head-to-head comparison of multiple amyloid PET radiotracers for Down syndrome clinical trials

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2025-03-19

Adults with Down syndrome carry high risk of developing Alzheimer’s disease and efforts to include this population in clinical trials remain limited. 4 key findings →

Design: longitudinal study Participants: 237 Evidence: moderate

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

A disease similarity approach identifies short-lived Niemann-Pick type C disease mice with accelerated brain aging as a novel mouse model for Alzheimer’s disease and aging research

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2024-04-23

Since its first description in 1906 by Dr. Alois Alzheimer, Alzheimer’s disease (AD) has been the most common type of dementia. 4 key findings →

Evidence: low

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

Chr21 protein-protein interactions: enrichment in products involved in intellectual disabilities, autism and Late Onset Alzheimer Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2019-12-12

Intellectual disability (ID) found in Down syndrome (DS), which is characterized by an extra copy of 234 genes on Chr21 is poorly understood. 4 key findings →

Evidence: low

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

Passive immunization reduces behavioral and neuropathological deficits in an alpha-synuclein transgenic model of Lewy body disease

⚠ Retracted — do not rely on it alzhub usefulness score 16 out of 100. PloS one 2011-04-29

Dementia with Lewy bodies (DLB) and Parkinson's Disease (PD) are common causes of motor and cognitive deficits and are associated with the abnormal accumulation of alpha-synuclein (α-syn). 4 key findings →

Evidence: low

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

Selective molecular alterations in the autophagy pathway in patients with Lewy body disease and in models of alpha-synucleinopathy

⚠ Retracted — do not rely on it alzhub usefulness score 16 out of 100. PloS one 2010-02-19

This study supports the notion that defects in the autophagy pathway and more specifically in mTor and Atg7 are associated with neurodegeneration in DLB cases and alpha-synuclein transgenic models and supports the possibility that modulators of the autophagy pathway might have potential therapeutic effects. 5 key findings →

Evidence: low

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

Directed conversion of Alzheimer's disease patient skin fibroblasts into functional neurons

⚠ Retracted — do not rely on it alzhub usefulness score 16 out of 100. Cell 2011-08-01

Directed conversion of mature human cells, as from fibroblasts to neurons, is of potential clinical utility for neurological disease modeling as well as cell therapeutics. 2 key findings →

Evidence: low

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

A head-to-head comparison of plasma biomarkers to detect biologically defined Alzheimer in a memory clinic

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2024-10-27

Blood-based biomarkers for Alzheimer’s disease (AD) have been widely studied, but direct comparisons of several biomarkers in clinical settings remain limited. 4 key findings →

Design: cross-sectional Participants: 197 Evidence: moderate

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

Antemortem α-Synuclein levels from neuron-derived extracellular vesicles identify Lewy Body pathology in Parkinson’s Disease and Alzheimer Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-08-05

These aggregated proteins contribute to the pathological and clinical heterogeneity of AD and are associated with a more rapid progression. 4 key findings →

Participants: 1,304 Evidence: low

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

Abnormalities in core AD biomarkers precede inflammatory and glial markers in CSF in Autosomal Dominant Alzheimer’s Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-04-01

Increasing evidence suggests that accurate prediction of Alzheimer’s disease (AD) symptom onset requires more than amyloid- and tau-centric biomarkers such as cerebrospinal fluid (CSF) Aβ42/40, total tau and p-tau181 and plasma p-tau217. 4 key findings →

Participants: 484 Evidence: low

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

Routine implementation of α-synuclein Seed Amplification Assays reveals high diagnostic performance and the limited value of Alzheimer disease fluid biomarkers for detecting α-synuclein co-pathology

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-04-23

In neurodegenerative diseases, the diagnostic value of α-synuclein seed amplification assay (αSAA) in routine clinical practice and its relationship with cognitive performance and fluid biomarkers remains incompletely characterized. 4 key findings →

Participants: 398 Evidence: moderate

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

↑ Change the filters

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