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.

Find studies

Showing 351–375 of 408 studies with an author at University of Southern California (US) (page 15 of 17) · 29,380 in the whole library · How the 0–100 score works

Download bibliography of these 408 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.

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.

Change detected by the MCI-CGIC was associated with baseline clinical severity and with change in clinical ratings over 6 and 12 months, supporting the validity of a CGIC approach in MCI. 5 key findings →

Evidence: high

Familism has been pointed out as a key value in Hispanic culture that may or may not be associated with caregiver distress. 4 key findings →

Evidence: low

Although DSCR1 (Adapt78) has been associated with successful adaptation to oxidative stress and calcium stress and with devastating diseases such as Alzheimer's and Down syndrome, no rationale for these apparently contradictory findings has been tested. 2 key findings →

Evidence: low

Alzheimer´s disease (AD) is a progressive neurodegenerative disorder of complex etiology, while Down syndrome (DS) is considered a genetically determined form of AD. 2 key findings →

Evidence: low

As in Alzheimer-disease (AD) brain, vacuolated muscle fibers of inclusion-body myositis (IBM) contain abnormally accumulated beta-amyloid precursor protein (beta APP), including its beta-amyloid protein epitope, and increased beta APP-751 mRNA. 4 key findings →

Evidence: low

Black participants had 2.883 times higher odds of developing dementia compared to Whites, while Hispanic participants had 1.230 times higher odds (not statistically significant). 5 key findings →

Participants: 3,495 Evidence: low

Artificial intelligence and neuroimaging enable accurate dementia prediction but often involve 'black box' models that can be difficult to trust. 5 key findings →

Evidence: low

The RCAN1 gene encodes three different protein isoforms: RCAN1-4, RCAN1-1L, and RCAN1-1S. RCAN1-1L is the RCAN1 isoform predominantly expressed in human brains. 2 key findings →

Evidence: low

In 2020, the Centers for Medicare and Medicaid Services reintroduced Alzheimer's disease and related dementias to its risk-adjustment payment model for Medicare Advantage (MA) plans. 5 key findings →

Evidence: low

Twenty-two studies (RCTs, non-RCTs, single arm and prospective trials) were included (n = 6-977; mean age: 72.0 years; 66.9% male). 5 key findings →

Evidence: low

We found notable differences in socio‐demographic and clinical characteristics, and utilization patterns in the year prior to death between decedents with dementia who were hospitalized in the last 30 days of life vs. those who were not. 4 key findings →

Participants: 6,299 Evidence: moderate

There is evidence of geographical variation in dementia[1], not all of which can be ascribed to genetic factors[2]. 1 key finding →

Participants: 568 Evidence: low

Obesity is associated with numerous adverse neural effects, including reduced neurogenesis, cognitive impairment, and increased risks for developing Alzheimer's disease (AD) and vascular dementia. 5 key findings →

Evidence: low

• APOE4 carriers exhibit cerebrovascular dysfunction. • Endothelial progenitor cells (EPC) represent cell populations involved in facilitating vascular repair. • In APOE4 carriers, EPC colony count is associated with cerebral small vessel disease. • EPC colony count may indicate activation of mechanisms which protect cerebrovascular function in APOE4 carriers prior to the development of cognitive decline. 4 key findings →

Participants: 109 Evidence: low

Among women, the number of years spent living with dementia for Whites, Blacks, U.S.-born Hispanics, and foreign-born Hispanics was 1.6, 3.9, 4.7, and 6.0 years, respectively. 3 key findings →

Evidence: low

The fMRI entropy classifier matched the tau PET model in accuracy and outperformed it in F1 score (0.64 vs. 0.61) and area under the curve (AUC; 0.73 vs. 0.67). 4 key findings →

Evidence: moderate

Spending at end of life (EOL) accounts for a large and growing share of healthcare expenditures in the US, and often reflects aggressive care with questionable value for dying patients. 2 key findings →

Evidence: low

↑ 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 29,380 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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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.

1,037 records (3.5% of the library) are not peer-reviewed — 964 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