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 5,601–5,625 of 10,985 studies · free to read (page 225 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.

Systemic immune challenges trigger and drive Alzheimer-like neuropathology in mice

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Journal of neuroinflammation 2012-07-02

Accumulating evidence suggests that neuroinflammation, mediated by the brain's innate immune system, contributes to AD neuropathology and exacerbates the course of the disease. 5 key findings →

Evidence: low

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

Developmental abnormalities and age-related neurodegeneration in a mouse model of Down syndrome

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1996-11-01

To study the pathogenesis of central nervous system abnormalities in Down syndrome (DS), we have analyzed a new genetic model of DS, the partial trisomy 16 (Ts65Dn) mouse. 1 key finding →

Evidence: low

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

Positron emission tomography of brain β-amyloid and τ levels in adults with Down syndrome

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Archives of neurology 2011-06-01

Consistent with neuropathological findings from postmortem studies, [(18)F]FDDNP positron emission tomography shows high binding levels in Down syndrome comparable to Alzheimer disease and greater levels than in members of a control group. 3 key findings →

Design: cross-sectional Participants: 19 Evidence: low

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

Plasma NT1-tau and Aβ42correlate with age and cognitive function in two large Down syndrome cohorts

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2023-03-10

Structured Abstract Introduction People with Down syndrome (DS) often develop Alzheimer disease (AD). 4 key findings →

Design: cross-sectional Participants: 85 Evidence: moderate

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

Tau pathology in Alzheimer disease and other tauopathies

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Biochimica et biophysica acta 2005-01-01

Just as neuronal activity is essential to normal brain function, microtubule-associated protein tau appears to be critical to normal neuronal activity in the mammalian brain, especially in the evolutionary most advanced species, the homo sapiens. 2 key findings →

Evidence: low

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

The neuropathology of traumatic brain injury

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Handbook of clinical neurology 2015-01-01

Traumatic brain injury, a leading cause of mortality and morbidity, is divided into three grades of severity: mild, moderate, and severe, based on the Glasgow Coma Scale, the loss of consciousness, and the development of post-traumatic amnesia. 3 key findings →

Evidence: low

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

Inhibition of heparin-induced tau filament formation by phenothiazines, polyphenols, and porphyrins

✓ Peer-reviewed alzhub usefulness score 49 out of 100. The Journal of biological chemistry 2004-12-17

Tau protein is the major component of the intraneuronal filamentous inclusions that constitute defining neuropathological characteristics of Alzheimer's disease and other tauopathies. 1 key finding →

Evidence: low

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

TAR DNA-binding protein 43 in neurodegenerative disease

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Nature reviews. Neurology 2010-03-16

In 2006, TAR DNA-binding protein 43 (TDP-43), a highly conserved nuclear protein, was identified as the major disease protein in amyotrophic lateral sclerosis (ALS) and in the most common variant of frontotemporal lobar degeneration (FTLD), FTLD-U, which is characterized by cytoplasmic inclusions that stain positive for ubiquitin but negative for tau and alpha-synuclein. 5 key findings →

Evidence: low

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

Accumulation of pathological tau species and memory loss in a conditional model of tauopathy

✓ Peer-reviewed alzhub usefulness score 49 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2007-04-01

Neurofibrillary tangles (NFTs) are a pathological hallmark of Alzheimer's disease and other tauopathies, but recent studies in a conditional mouse model of tauopathy (rTg4510) have suggested that NFT formation can be dissociated from memory loss and neurodegeneration. 3 key findings →

Evidence: low

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

The presenilin hypothesis of Alzheimer's disease: evidence for a loss-of-function pathogenic mechanism

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2006-12-29

Dominantly inherited mutations in the genes encoding presenilins (PS) and the amyloid precursor protein (APP) are the major causes of familial Alzheimer's disease (AD). 1 key finding →

Evidence: low

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

Proteomic and functional analyses reveal a mitochondrial dysfunction in P301L tau transgenic mice

✓ Peer-reviewed alzhub usefulness score 49 out of 100. The Journal of biological chemistry 2005-04-14

Transgenic mice overexpressing the P301L mutant human tau protein exhibit an accumulation of hyperphosphorylated tau and develop neurofibrillary tangles. 5 key findings →

Evidence: low

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

Mechanisms of Parkinson's disease linked to pathological alpha-synuclein: new targets for drug discovery

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Neuron 2006-10-01

Classic Parkinson's disease (PD) is characterized by fibrillar alpha-synuclein inclusions known as Lewy bodies in the substantia nigra, which are associated with nigrostriatal degeneration. 1 key finding →

Evidence: low

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

Physiological functions and pathobiology of TDP-43 and FUS/TLS proteins

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Journal of neurochemistry 2016-06-15

The multiple roles played by RNA binding proteins in neurodegeneration have become apparent following the discovery of TAR DNA binding protein 43 kDa (TDP-43) and fused in sarcoma/translocated in liposarcoma (FUS/TLS) involvement in amyotrophic lateral sclerosis and frontotemporal lobar dementia. 5 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 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