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.

Precision nutrition is a tailored dietary approach that considers an individual’s genetic and metabolic profile, lifestyle factors, and specific nutritional needs to improve health and potentially modify disease progression. 5 key findings →

Design: narrative review Evidence: low

Apolipoprotein E-4 (APOE-4), serotonin transporter gene (SLC6A4), and single nucleotide polymorphisms (SNPs) of glucocerebrosidase (GBA) are some of the main altered genes in AD, PDD and DLB. 5 key findings →

Evidence: low

Full or partial trisomy of human chromosome 21 results in dysregulation of gene expression, leading to the manifestation of specific phenotypes described in individuals with Down syndrome (DS). 3 key findings →

Evidence: low

Introducción: La enfermedad de Alzheimer se considera una de las patologías neurodegenerativas de mayor impacto en la salud pública, con una prevalencia y tasa de mortalidad en incremento. 5 key findings →

Evidence: low

Introducción. La enfermedad de Alzheimer (EA) es una condición neurodegenerativa progresiva caracterizada por el deterioro cognitivo, la acumulación de beta-amiloide y la neuroinflamación. La tecnología CRISPR/Cas9 ha emergido como una herramienta prometedora para investigar y, potencialmente, tratar la EA, permitiendo ediciones precisas del genoma y la modulación de la expresión génica. 5 key findings →

Evidence: low

Chronic psychological stress is a well-known risk factor for neurodegenerative diseases including Alzheimer disease (AD), yet the underlying mechanisms remain unclear. 4 key findings →

Evidence: low

The repeated inability of Aβ therapies to pass clinical tests in sporadic AD points to the complexity of the disease and indicates that earlier or more interventions could be necessary. 5 key findings →

Evidence: low

The human brain is one of the most metabolically active tissues in the body, due in large part to the activity of trillions of synaptic connections. 1 key finding →

Evidence: low

Benzene-1,3-disulfonic acid exhibited strong binding to the Arg136-containing pocket with a top docking score of -5.93 kcal/mol and an estimated inhibition constant (Ki) of 44.6 µmol. 5 key findings →

Evidence: low

One of the biggest health issues of the twenty-first century is Alzheimer's disease (AD), which is the most prevalent cause of dementia. 1 key finding →

Evidence: low

A Doença de Alzheimer (DA) é uma enfermidade neurodegenerativa progressiva e a principal causa de demência em idosos, representando cerca de 60 a 70% dos casos. 5 key findings →

Evidence: low

A Doença de Alzheimer (DA) é uma patologia neurodegenerativa de caráter progressivo, marcada pela deterioração gradual das funções cognitivas e motoras do indivíduo, com o consequente comprometimento da memória, da linguagem e do comportamento. 5 key findings →

Evidence: low

La presente revisión bibliográfica analiza el papel de la genética clínica en el diagnóstico y pronóstico de la enfermedad de Alzheimer, con un énfasis especial en el contexto ecuatoriano. 5 key findings →

Evidence: low

Alzheimer disease involves interacting mechanisms that include amyloid-beta accumulation, abnormal tau phosphorylation and aggregation, cholinergic dysfunction, synaptic degeneration, neuronal loss, neuroinflammation, vascular pathology, and genetic susceptibility. 5 key findings →

Design: narrative review Evidence: low

This article tells us how modern biotechnology and AI are redefining Alzheimer’s disease through early detection, advanced biomarkers, and innovative treatments like lecanemab. 5 key findings →

Evidence: low

Alzheimer disease (AD) is a progressive neurodegenerative disease and the most common cause of dementia in the world, which has a gradual deterioration of memory, thinking and autonomy. 2 key findings →

Evidence: low

Alzheimer disease (AD) is the neurodegenerative condition that occurs in the elderly population above 65 years old and is the major cause of dementia. 5 key findings →

Evidence: low

Alzheimer's disease (AD) is a neurological condition that worsens over time and is characterised by tau tangles and amyloid plaques. 2 key findings →

Evidence: low

Descobertas e avanços do sequenciamento de próxima geração na doença de Alzheimer

✓ Peer-reviewed alzhub usefulness score 27 out of 100. BioSCIENCE 2025-09-05

Introdução: O sequenciamento de nova geração (NGS) tem revolucionado a compreensão da doença de Alzheimer (DA), desvendando biomarcadores genéticos e transcriptômicos que aprimoram a estrutura ATN (beta-amiloide, Tau, neurodegeneração). 5 key findings →

Evidence: low

From across this tag

10 of the 3,521 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 10. The same 10 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