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.

CSF samples were retrospectively collected from 253 subjects recruited at Peking Union Medical College Hospital, Xuanwu Hospital Capital Medical University, and Beijing Tiantan Hospital between July 2013 and September 2019. 4 key findings →

Participants: 253 Evidence: moderate

Plasma glial fibrillary acidic protein (GFAP) has emerged as a promising biomarker of astrocytic reactivity in preclinical Alzheimer´s Disease (AD). 4 key findings →

Participants: 143 Evidence: low

DNA methylation has been shown to play a crucial role in many diseases, including Alzheimer's disease (AD). 4 key findings →

Design: longitudinal study Evidence: moderate

Serum levels of S100B and NSE proteins in Alzheimer's disease patients

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of neuroinflammation 2010-01-27

Alzheimer's disease is the most common dementia in the elderly, and the potential of peripheral biochemical markers as complementary tools in the neuropsychiatric evaluation of these patients has claimed further attention. 4 key findings →

Evidence: low

A significant portion of our risk for dementia in old age is associated with lifestyle factors (diet, exercise, and cardiovascular health) that are modifiable, at least in principle. 4 key findings →

Evidence: low

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by brain deposition of senile (neuritic) plaques containing amyloid-β, neurofibrillary tangles, synaptic loss, neuroinflammation, and overexpression of arachidonic acid (AA, 20:4n-6) metabolizing enzymes. 4 key findings →

Evidence: low

Using a large and diverse community‐based cohort, we demonstrate that ethno‐racial differences in AD‐specific plasma biomarkers are, in part, due to modifiable health and comorbidity factors. 2 key findings →

Participants: 931 Evidence: moderate

Fourteen participants (21.5%) converted to MCI, and 24 (36.9%) were classified as Prog-1.Plasma biomarkers did not show consistent predictive performance across predefined endpoints (all p>0.05), although NfL demonstrated modest discrimination for MCI conversion (area under the curve [AUC] 0.686, p=0.008).Hippocampal volume demonstrated significant discriminative performance for MCI conversion (AUC 0.765, p=0.016) and Prog-1 (AUC 0.933, p<0.001).For Prog-2, hippocampal volume showed high discrimination (AUC 0.952, p<0.001).WMH grade also demonstrated significant discrimination for MCI conversion (AUC 0.835, p<0.001) and Prog-1 (AUC 0.857, p<0.001).Bootstrap analyses (1,000 iterations) tended to show higher AUC estimates for imaging markers compared with plasma biomarkers. 2 key findings →

Evidence: moderate

High Resolution Image Download MS PowerPoint Slide Responders (R) and Non-Responders (NR) to lymphatic-venous anastomosis (LVA) surgery for relief of cognitive impairment show significant difference in their p-tau181/Aβ42 ratios via enzyme-linked immunosorbent assay (ELISA) of their cerebrospinal fluid (CSF). 3 key findings →

Participants: 43 Evidence: moderate

Retinal biomarkers for the risk of Alzheimer’s disease and frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Frontiers in Aging Neuroscience 2025-01-10

Our findings provide preliminary empirical support for a relationship between prodromal changes in retinal layers and a higher risk of AD or FTD, suggesting that macular OCT may serve as a non-invasive, sensitive biomarker of high-risk years before the onset of dementia. 3 key findings →

Participants: 148 Evidence: low

Amyloid‐reactive T cell polyfunctional response distinguishes MCI from normal aging and could serve as a novel MCI biomarker. 4 key findings →

Evidence: moderate

Mitochondrial oxidative stress and neuroinflammation are involved in the onset and progression of Alzheimer's disease (AD). 5 key findings →

Evidence: low

In PD patients, a decrease in [ 18 F]DOPA PET retention correlated with disease duration as well as CSF neurodegenerative and synaptic biomarkers but not with inflammatory biomarkers or [ 18 F]RO948 PET midbrain off-target retention. 2 key findings →

Participants: 623 Evidence: low

Plasma ptau217 has strong diagnostic performance in distinguishing CSF biomarker-defined AD in a clinically relevant, younger cohort of people with symptoms, adding further weight for a simple diagnostic blood test for AD as a cause of a patient's symptoms. 2 key findings →

Evidence: moderate

The relationship between the presence and severity of AIDS dementia complex (ADC) and the levels of human immunodeficiency virus type 1 (HIV-1) RNA in cerebrospinal fluid (CSF) were assessed. 2 key findings →

Evidence: low

These data provide potential insights into the biology of CSF in AD and MCI progression and provide a novel tool for AD researchers and clinicians working to improve diagnostic accuracy, evaluation of treatment efficacy, and early diagnosis. 3 key findings →

Evidence: low

Analyses of cerebrospinal fluid (CSF) biomarkers (β-amyloid protein, total tau protein, and hyperphosphorylated tau protein) are part of the diagnostic criteria of Alzheimer disease. 4 key findings →

Evidence: low

In the last decades, an important role of cerebrospinal fluid (CSF) biomarkers for Alzheimer disease (AD) diagnosis has emerged. 4 key findings →

Participants: 96 Evidence: low

In vivo Prevalence of Alzheimer Biomarkers in Dementia with Lewy Bodies

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Dementia and geriatric cognitive disorders 2019-07-16

Neuropathological studies indicate concomitant Alzheimer's disease (AD) pathology in patients with dementia with Lewy bodies (DLB). 4 key findings →

Participants: 38 Evidence: low

This observational study included 290 cognitively unimpaired (CU) participants with a family history (FH) of clinically diagnosed sporadic AD (age 49-73 years) from the Alzheimer's and Families (ALFA) study. [ 18 F]flutemetamol-PET standardized uptake value ratios, CSF β-amyloid 42/40 ratio, and phosphorylated tau were used as AD biomarkers. 4 key findings →

Participants: 290 Evidence: low

From across this tag

9 of the 829 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 9. The same 9 appear here every time.

↑ 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