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

28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–22 of 22 studies with an author at Boston Children's Hospital (US) · free to read · 28,580 in the whole library · How the 0–100 score works

Download bibliography of these 22 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.

Other institutions

From OpenAlex; 14,058 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.

A cerebrospinal fluid synaptic protein biomarker for prediction of cognitive resilience versus decline in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 77 out of 100. Nature medicine 2025-03-31

Rates of cognitive decline in Alzheimer's disease (AD) are extremely heterogeneous. 1 key finding →

Design: case-control study Participants: 3,397 Evidence: moderate

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

Artificial intelligence for diagnostic and prognostic neuroimaging in dementia: A systematic review

✓ Peer-reviewed alzhub usefulness score 71 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2023-08-10

The literature has several methodological limitations including lack of sufficient algorithm development descriptions and standard definitions. 1 key finding →

Participants: 255 Evidence: moderate

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

Designing and implementing the IDEAL Study: A randomized clinical trial of APOE genotype disclosure for late-onset Alzheimer's disease in an urban Latino population

✓ Peer-reviewed alzhub usefulness score 67 out of 100. Alzheimer's & dementia (New York, N. Y.) 2024-10-01

We sent invitations to 91,433 households; 5542 (6.1%) responded, 2120 completed the Baseline Survey (78.5% online; 21.5% via computer-assisted telephone interview), and 2087 were deemed eligible, yielding a response rate of 2.3%. 2 key findings →

Design: randomized controlled trial Participants: 374 Evidence: high

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

Inclusion body myopathy associated with Paget disease of bone and frontotemporal dementia is caused by mutant valosin-containing protein

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Nature genetics 2004-03-21

Inclusion body myopathy associated with Paget disease of bone and frontotemporal dementia (IBMPFD) is a dominant progressive disorder that maps to chromosome 9p21.1-p12. 4 key findings →

Evidence: low

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

Psychological impacts of APOE genotype disclosure among Latinos in New York City: a randomized controlled trial

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Alzheimer s & Dementia 2026-09-01

Disclosure (N = 194) and non-disclosure (N = 180) groups did not differ on IGT-AD (mean disclosure-non-disclosure difference [MD] at 6 weeks: -1.5, p = 0.14; 9 months: -1.2, p = 0.35; 15 months: -2.0, p = 0.07), IES-R (MD at 6 weeks: 0.00, p = 0.98; 9 months: 0.01, p = 0.84; 15 months: 0.03, p = 0.64), or change in secondary outcomes. 4 key findings →

Design: randomized controlled trial Participants: 194 Evidence: high

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

Molecular features of human pathological tau distinguish tauopathy-associated dementias

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Cell 2026-01-29

In Alzheimer's disease (AD), pathological tau protein shows a progressive accumulation of post-translational modifications (PTMs), reflecting disease severity, progression, and prion-like activity. 5 key findings →

Evidence: low

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

Cryptic splicing in synaptic and membrane excitability genes links TDP-43 loss to neuronal dysfunction

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Science Translational Medicine 2026-06-03

Using human stem cell-derived neurons, we show that TDP-43 reduction induces cryptic splicing and downregulation of these genes, resulting in impaired excitability and synaptic transmission. 1 key finding →

Evidence: low

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

TDP-43 accumulation in inclusion body myopathy muscle suggests a common pathogenic mechanism with frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Journal of neurology, neurosurgery, and psychiatry 2008-10-01

TAR DNA binding protein-43 (TDP-43) is found in ubiquitinated inclusions (UBIs) in some frontotemporal dementias (FTD-U). 4 key findings →

Evidence: low

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

Nerve growth factor increases mRNA levels for the prion protein and the beta-amyloid protein precursor in developing hamster brain

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1988-12-01

Deposition of amyloid filaments serves as a pathologic hallmark for some neurodegenerative disorders. 1 key finding →

Evidence: low

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

VCP disease associated with myopathy, Paget disease of bone and frontotemporal dementia: review of a unique disorder

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Biochimica et biophysica acta 2008-09-18

Inclusion body myopathy (IBM) associated with Paget disease of the bone (PDB) and frontotemporal dementia (FTD) (now called IBMPFD), is a progressive autosomal dominant disorder that was recently identified as being caused by mutations in the VCP (p97 or CDC48) gene which plays a key role in the ubiquitin-proteasome dependent degradation of cytosolic proteins and in the retro translocation of misfolded proteins from the endoplasmic reticulum into the cytoplasm. 4 key findings →

Evidence: low

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

Saikosaponin C ameliorates tau-related pathology by modulating oxidative stress and MAPK axis in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Journal of Ethnopharmacology 2025-07-02

It has been demonstrated to have neuroprotective effects in cellular models of neurodegenerative diseases; however, its precise mechanism of action in alleviating tau pathology in Alzheimer's disease (AD), as well as its potential to improve cognitive deficits in animal models, has not yet been elucidated. 3 key findings →

Evidence: low

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

CD33 and clusterin interact biophysically and genetically to modulate Alzheimer risk

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Nature Communications 2026-07-17

We report the results of structural, functional and genetic studies on the CD33 sialic acid- binding receptor that reveal how non-coding variants in CD33 alter risk for Alzheimer’s disease (AD). 2 key findings →

Evidence: low

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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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.

1,034 records (3.6% 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