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 1–24 of 24 studies with an author at National Center of Neurology and Psychiatry (JP) · 27,380 in the whole library · How the 0–100 score works

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; 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.

SORL1 is genetically associated with late-onset Alzheimer's disease in Japanese, Koreans and Caucasians

✓ Peer-reviewed alzhub usefulness score 69 out of 100. PloS one 2013-04-02

To discover susceptibility genes of late-onset Alzheimer's disease (LOAD), we conducted a 3-stage genome-wide association study (GWAS) using three populations: Japanese from the Japanese Genetic Consortium for Alzheimer Disease (JGSCAD), Koreans, and Caucasians from the Alzheimer Disease Genetic Consortium (ADGC). 1 key finding →

Participants: 1,008 Evidence: low

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

Clarity AD: Asian regional analysis of a phase III trial of lecanemab in early Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 58 out of 100. The Journal of Prevention of Alzheimer s Disease 2025-04-06

Of the total of 1795 subjects randomized in Clarity AD, 294 subjects were in the Asian region (Japan:152; Korea:129; Singapore:13). 5 key findings →

Design: clinical trial Participants: 294 Evidence: high

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

Japanese and North American Alzheimer's Disease Neuroimaging Initiative studies: Harmonization for international trials

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2018-05-09

These results support the feasibility of bridging of clinical trials in the prodromal stage of AD between Asia and western countries. 3 key findings →

Participants: 75 Evidence: low

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

Automatic voxel-based morphometry of structural MRI by SPM8 plus diffeomorphic anatomic registration through exponentiated lie algebra improves the diagnosis of probable Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 49 out of 100. AJNR. American journal of neuroradiology 2012-02-02

This software program with application of SPM8 plus DARTEL to VBM provides a high performance for AD diagnosis by using MRI. 1 key finding →

Participants: 45 Evidence: low

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

MMSE–CDR‐SB residual as an exploratory indicator of deviation from an Alzheimer's disease–typical cognitive–functional pattern

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring 2026-07-01

The MMSE–CDR‐SB residual may help flag less AD‐typical presentations for further etiologic evaluation, but cannot be interpreted as a pathology‐specific marker due to substantial overlap across diagnostic groups. 2 key findings →

Participants: 1,981 Evidence: moderate

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

Cellular co-localization of phosphorylated tau- and NACP/alpha-synuclein-epitopes in lewy bodies in sporadic Parkinson's disease and in dementia with Lewy bodies

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Brain research 1999-10-01

The precursor of the non-Abeta-component of Alzheimer's disease (AD) amyloid (NACP, alpha-synuclein) aggregates into insoluble filaments of Lewy bodies (LBs) in Parkinson's disease (PD) and dementia with LBs (DLB). 2 key findings →

Evidence: low

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

Corticonigral degeneration with neuronal achromasia presenting with primary progressive aphasia: ultrastructural and immunocytochemical studies

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of the neurological sciences 1994-12-01

We describe a clinico-pathological variant of a degenerative disorder involving Broca's, Wernicke's, and supplementary motor areas, which presented as primary progressive aphasia, dysarthria, bucco-facial apraxia, and hearing loss as initial symptoms, followed by organic personality changes. 4 key findings →

Evidence: low

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

Elevated expression of beta-site amyloid precursor protein cleaving enzyme 2 in brains of patients with Down syndrome

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Neuroscience letters 2002-06-01

The gene encoding the beta-site amyloid precursor protein cleaving enzyme 2 (BACE2) has been determined to be located on the long arm of chromosome 21 at 21q22.3. 5 key findings →

Evidence: low

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

Immunohistochemical characterization of microglia in Nasu-Hakola disease brains

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Neuropathology : official journal of the Japanese Society of Neuropathology 2010-12-01

Nasu-Hakola disease (NHD) is a rare autosomal recessive disorder, characterized by progressive presenile dementia and formation of multifocal bone cysts, caused by genetic mutations of DNAX-activation protein 12 (DAP12) or triggering receptor expressed on myeloid cells 2 (TREM2). 4 key findings →

Evidence: low

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

Characteristic developmental expression of amyloid beta40, 42 and 43 in patients with Down syndrome

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain & development 2003-04-01

We immunohistochemically studied the expression of beta-amyloid precursor protein (APP), Abeta40, Abeta42, and Abeta43 in the frontal lobes of 20 Down syndrome (DS) patients and 13 controls. 5 key findings →

Evidence: low

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

Developmental immunohistochemistry of growth inhibitory factor in normal brains and brains of patients with Down syndrome

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Pediatric neurology 1997-09-01

Growth inhibitory factor, a new metallothioneinlike protein, was investigated at postmortem examination in the brains of 18 patients with Down syndrome ranging in age from 18 weeks gestation to 50 years of age and in 20 age-matched normal controls by developmental immunohistochemistry. 5 key findings →

Participants: 18 Evidence: low

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

Astrocytic deformity and globular structures are characteristic of the brains of patients with aceruloplasminemia

✓ Peer-reviewed alzhub usefulness score 34 out of 100. Journal of neuropathology and experimental neurology 2002-12-01

Aceruloplasminemia is an interesting disease, the study of which helps elucidate how iron-induced oxidative stress is involved in neuronal cell death. 2 key findings →

Evidence: low

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

Developmental and aging changes in the expression patterns of beta-amyloid in the brains of normal and Down syndrome cases

✓ Peer-reviewed alzhub usefulness score 32 out of 100. Brain & development 1990-01-01

Immunohistochemical staining with polyclonal antibodies to synthetic amyloid (residues 1-28 of A4) was performed on normal and Down syndrome brains from fetuses to adults. 1 key finding →

Evidence: low

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

High expression on Kunitz-type protease inhibitor-containing substances in the cerebral vessels of patients with Down syndrome

✓ Peer-reviewed alzhub usefulness score 28 out of 100. The Tohoku journal of experimental medicine 1994-11-01

Down syndrome (DS) brains, from 19 gestational weeks to 50 years of age were studied by immunohistochemical methods with a polyclonal antibody against synthetic peptide comprising part of the Kunitz-type protease inhibitor (KPI) domain of Alzheimer disease amyloid precursor protein (APP), residues 301 to 323 of APP 770. 1 key finding →

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. 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 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