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

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 6,076–6,100 of 27,146 studies marked Peer-reviewed (page 244 of 1086) · 28,180 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; 13,658 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.

TDP-43 and FUS in amyotrophic lateral sclerosis and frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 57 out of 100. The Lancet. Neurology 2010-10-01

Abnormal intracellular protein aggregates comprise a key characteristic in most neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 5 key findings →

Evidence: low

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

RNA toxicity from the ALS/FTD C9ORF72 expansion is mitigated by antisense intervention

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Neuron 2013-10-01

A hexanucleotide GGGGCC repeat expansion in the noncoding region of the C9ORF72 gene is the most common genetic abnormality in familial and sporadic amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 1 key finding →

Evidence: low

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

RAN proteins and RNA foci from antisense transcripts in C9ORF72 ALS and frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2013-11-18

The finding that a GGGGCC (G4C2) hexanucleotide repeat expansion in the chromosome 9 ORF 72 (C9ORF72) gene is a common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) links ALS/FTD to a large group of unstable microsatellite diseases. 3 key findings →

Evidence: low

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

TDP-43 repression of nonconserved cryptic exons is compromised in ALS-FTD

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Science (New York, N.Y.) 2015-08-01

Cytoplasmic aggregation of TDP-43, accompanied by its nuclear clearance, is a key common pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementia (ALS-FTD). 2 key findings →

Evidence: low

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

Animal models of neurodegenerative diseases

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Nature neuroscience 2018-09-24

Animal models of adult-onset neurodegenerative diseases have enhanced the understanding of the molecular pathogenesis of Alzheimer's disease, Parkinson's disease, frontotemporal dementia, and amyotrophic lateral sclerosis. 4 key findings →

Evidence: low

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

3D maps from multiple MRI illustrate changing atrophy patterns as subjects progress from mild cognitive impairment to Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Brain : a journal of neurology 2007-05-28

Voxel-based morphometry (VBM) was used to assess patterns of grey matter atrophy in the aMCI subjects at each time-point compared to the control group. 4 key findings →

Evidence: moderate

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

Ventricular enlargement as a possible measure of Alzheimer's disease progression validated using the Alzheimer's disease neuroimaging initiative database

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Brain : a journal of neurology 2008-07-11

Ventricular enlargement may be an objective and sensitive measure of neuropathological change associated with mild cognitive impairment (MCI) and Alzheimer's disease (AD), suitable to assess disease progression for multi-centre studies. 2 key findings →

Participants: 152 Evidence: low

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

Outcomes of mild cognitive impairment by definition: a population study

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Archives of neurology 2011-06-01

As ascertained by several operational definitions, MCI is a heterogeneous entity at the population level but progresses to dementia at rates higher than in normal elderly individuals. 1 key finding →

Participants: 1,982 Evidence: moderate

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

Accelerated progression from mild cognitive impairment to dementia in people with diabetes

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Diabetes 2010-08-16

Diabetes and pre-diabetes substantially accelerate the progression from MCI to dementia, and anticipate dementia occurrence by more than 3 years in people with MCI. 3 key findings →

Participants: 302 Evidence: moderate

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

Late-life depression as a risk factor for mild cognitive impairment or Alzheimer's disease in 30 US Alzheimer's disease centers

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Journal of Alzheimer's disease : JAD 2012-01-01

Identification of potentially modifiable risk factors for cognitive deterioration is important. 5 key findings →

Participants: 5,607 Evidence: low

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

Identification and validation of novel cerebrospinal fluid biomarkers for staging early Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 57 out of 100. PloS one 2011-01-12

These six markers describe six clinicopathological stages from cognitive normalcy to mild dementia, including stages defined by increased risk of cognitive decline. 1 key finding →

Participants: 24 Evidence: moderate

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

The rate of conversion of mild cognitive impairment to dementia: predictive role of depression

✓ Peer-reviewed alzhub usefulness score 57 out of 100. International journal of geriatric psychiatry 2007-06-01

We conclude that conversion rate from MCI to DSM-IIIR dementia was 21.9% over a period of 3 years. 4 key findings →

Design: longitudinal study Participants: 105 Evidence: moderate

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

Cerebrospinal fluid tau and beta-amyloid 42 proteins identify Alzheimer disease in subjects with mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Archives of neurology 2002-11-01

Our results indicate that altered tau and Abeta42 concentrations may be detectable in subjects who are clinically diagnosed as having MCI but demonstrate the pathological changes of AD. 5 key findings →

Design: longitudinal study Participants: 28 Evidence: moderate

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

↑ 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 (3.7% 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