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

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.

The double-cutoff approach revealed high confidence for interpreting scans as negative when Centiloid values were lower than 11 (95% CI, 9-13; I2 = 95%) and interpreting scans as positive if Centiloid values were higher than 26 (95% CI, 24-28; I2 = 95%). 3 key findings →

Design: meta-analysis Participants: 49,227 Evidence: high

Decades of research have revealed numerous risk factors for mental disorders beyond genetics, but their consistency and magnitude remain uncer-tain. 1 key finding →

Design: meta-analysis Participants: 176 Evidence: high

SGLT2 Inhibitor Use and Risk of Dementia and Parkinson Disease Among Patients With Type 2 Diabetes

✓ Peer-reviewed alzhub usefulness score 70 out of 100. Neurology 2024-09-18

In this nationwide population-based study, SGLT2i use significantly reduced the risks of neurodegenerative disorders in patients with type 2 diabetes independent of various factors including comorbidities and bioclinical parameters. 5 key findings →

Design: cohort Participants: 358,862 Evidence: moderate

Higher educational level (standardized β = 0.23, P Conclusions and relevance Results of this study suggest that women and young patients with AD have relative preservation of brain structure when exposed to neocortical pathological tau. 3 key findings →

Design: cross-sectional Participants: 260 Evidence: moderate

In the UGOT cohort, the optimal cutoff improved diagnostic accuracy compared with the standard single cutoff, particularly in CKD and anemia (CKD: from 0.65; 95% CI, 0.57-0.72; to 0.83; 95% CI, 0.76-0.89; anemia: from 0.80; 95% CI, 0.76-0.84; to 0.86; 95% CI, 0.82-0.90), with consistent findings in the Roche cohort. 4 key findings →

Design: cross-sectional Participants: 2,571 Evidence: moderate

Temporal Dynamics and Biological Variability of Alzheimer Biomarkers

✓ Peer-reviewed alzhub usefulness score 65 out of 100. JAMA neurology 2025-02-17

Among the plasma biomarkers, phosphorylated tau (p-tau) 217 exhibited the highest concordance rate with Aβ (2326 of 2571 [90.5%]) and tau (100 of 120 [83.3%]) PET. 4 key findings →

Design: cohort study Participants: 2,611 Evidence: moderate

A total of 807 K-ROAD participants (median age 72.0 years, 58.7% female) and 230 ADNI participants (median age 70.9 years, 49.1% female) were analyzed. 5 key findings →

Design: cohort study Participants: 807 Evidence: moderate

To develop a new method for measuring Alzheimer's disease (AD)-specific similarity of cortical atrophy patterns at the individual-level, we employed an individual-level machine learning algorithm. 5 key findings →

Design: longitudinal study Participants: 473 Evidence: moderate

In contrast to no change in global cortical SUVR in the CU- and CU+ groups during the 2-y period, global cortical SUVR increased by 0.06 (2.9%) in the MCI+ group and 0.19 (8.0%) in the DEM+ group at follow-up. 5 key findings →

Design: cross-sectional Participants: 107 Evidence: moderate

Anatomical heterogeneity of Alzheimer disease: based on cortical thickness on MRIs

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Neurology 2014-10-24

This cluster analysis of cortical thickness of the entire brain showed that AD dementia in the earlier stages can be categorized into various anatomical subtypes, with distinct clinical features. 5 key findings →

Participants: 52 Evidence: low

A meta-analysis using a random-effects model was performed to calculate the pooled standardized mean differences between overall symptoms and each type of symptom. 4 key findings →

Design: systematic review Evidence: high

Amyotrophic lateral sclerosis-frontotemporal dementia (ALS-FTD) constitutes a devastating disease spectrum characterized by 43-kDa TAR DNA-binding protein (TDP-43) pathology. 4 key findings →

Evidence: low

The advent of anti-amyloid monoclonal antibody (mAb) therapies represents a paradigm shift in the treatment of Alzheimer's disease (AD), from symptomatic relief to disease modification. 5 key findings →

Design: randomized controlled trial Evidence: high

Most patients with svMCI do not exhibit substantial amyloid burden, and CVD does not increase β-amyloid burden as measured by amyloid imaging. 5 key findings →

Design: cross-sectional Participants: 95 Evidence: low

Our findings suggest that poor chewing ability is associated with cognitive impairment or dementia in the elderly living in rural area. 4 key findings →

Design: cross-sectional Participants: 295 Evidence: low

We conducted a retrospective cohort study using the National Health Insurance Database in South Korea. 5 key findings →

Design: cohort study Evidence: moderate

Alzheimer disease (AD) is associated with an increase in the brain of the 18-kDa translocator protein (TSPO), which is overexpressed in activated microglia and reactive astrocytes. 4 key findings →

Evidence: low

There was an age-related increase in both 18 F-AV-1451 binding in the basal ganglia and R 2 * values in the putamen in both the controls and the Alzheimer disease/mild cognitive impairment patients. 18 F-AV-1451 binding in the basal ganglia increased with R 2 * values. 3 key findings →

Participants: 61 Evidence: low

High LDL-C (≥160 mg/dL) increased AD risk across all groups {hazard ratio (HR): 1.23 [95% confidence interval (CI): 1.10-1.38],p<0.001;HR: 1.45 (95% CI: 1.08-1.93),p=0.013;HR: 1.25 (95% CI: 1.10-1.42),p<0.001, respectively}, whereas low LDL-C (<70 mg/dL) showed higher VD risk in those not taking cholesterol-lowering medication [HR: 3.02 (95% CI: 1.73-5.27),p<0.001].Low HDL-C (≤40 mg/dL) was associated with increased AD and VD risk in non-users. 2 key findings →

Design: cohort study Evidence: moderate

Atrophy patterns in cerebral amyloid angiopathy with and without cortical superficial siderosis

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Neurology 2018-04-20

Our findings imply that the current version of the Boston criteria may not be sufficient enough to remove non-CAA cases from a cognitively impaired population, especially in the absence of cSS. 4 key findings →

Participants: 27 Evidence: low

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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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.

1,034 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