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 26–50 of 59 studies in Preprints.org (page 2 of 3) · 27,380 in the whole library · How the 0–100 score works

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.

From Dementia Prevention Literacy to Preventive Agency: A Proposed Theoretical Framework for Translating Knowledge into Action

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-20

Dementia prevention education increasingly seeks to translate evidence about modifiable risk factors into meaningful public engagement and preventive action. 5 key findings →

Evidence: low

The increasing prevalence of neurodegenerative diseases (NDs), especially Alzheimer's and Parkinson's, is a major public health concern in the Gulf countries (GCs) due to the rapid increase in life expectancy and population aging. 1 key finding →

Evidence: low

Proteomic Signatures of Vulnerability Across Late-Life Depression, Frailty, and Neurodegeneration

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-20

Late-life depression (LLD) is increasingly recognized as a complex multisystem disorder associated with accelerated biological aging, impaired physiological resilience, frailty, and an increased risk of cognitive decline and dementia. 3 key findings →

Evidence: low

Cortisol is primarily synthesized by the adrenal glands, but also within specific tissues via a distinct enzymatic pathway. 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyses the synthesis of cortisol within cells to create local higher cortisol environments in those organs where it is highly expressed such as the liver and brain. 4 key findings →

Participants: 247 Evidence: low

Traumatic Brain Injury, Chronic Traumatic Encephalopathy, and Alzheimer's Disease: Overlapping Phenotypes and Associations

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-09-14

Traumatic brain injury (TBI), chronic traumatic encephalopathy (CTE), and Alzheimer's disease (AD) share several neuropathophysiological mechanisms, including axonal injury, neuroinflammation, and abnormal protein aggregation, which may contribute to overlapping clinical manifestations. 1 key finding →

Evidence: low

Launched in 2010 by the National Institutes of Health, the Human Connectome Project (HCP) represents a foundational initiative in systems neuroscience, designed to map the structural and functional architecture of the human brain. 2 key findings →

Design: longitudinal study Evidence: moderate

However, increasing evidence indicates that systemic metabolic dysfunction, chronic inflammation, intestinal dysbiosis, hepatic abnormalities, and barrier impairment may substantially influence disease susceptibility and progression. 1 key finding →

Design: longitudinal study Evidence: moderate

Pantethine and Neurodegeneration: A Coenzyme A-Centered Framework Linking Metabolism, Neuroinflammation, and Mitochondrial Dysfunction

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-23

Neurodegenerative diseases are a growing global health burden associated with aging and characterized by progressive neuronal dysfunction, metabolic failure, mitochondrial impairment, oxidative stress, and chronic neuroinflammation. 1 key finding →

Design: narrative review Evidence: low

Protective or Pathogenic? Microglial Responses at the Intersection of Amyloid-β, Tau, and Neuroinflammation in Alzheimer’s Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-20

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β (Aβ) accumulation, pathological tau aggregation, and neuronal loss. 1 key finding →

Evidence: low

Bee venom (BV) contains bioactive peptides with potent antioxidant, anti-inflammatory, and neuroprotective properties, yet its direct therapeutic use is limited by cytotoxicity, instability, and uncontrolled release. 1 key finding →

Evidence: low

The Gut-Brain Axis Mechanism in Alzheimer’s Disease: From Animal Models to Clinical Translation and Innovative Treatment Strategies

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-07-30

Research on gut microbiota in Alzheimer’s disease (AD) has progressed from observational correlations to the validation of causal relationships. 3 key findings →

Evidence: high

This review examines nanocrystal-based theranostic platforms as a promising method to overcome the blood-brain barrier (BBB) in neurodegenerative diseases like Alzheimer’s and Parkinson’s. These neurological diseases involve gradual protein misfolding and aggregation, causing neuronal damage and loss. 1 key finding →

Evidence: low

Clinical Efficacy of Comprehensive Geriatric Assessment in Patients Undergoing Hemodialysis: A Retrospective Observational Study

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-07-06

Functional decline, as assessed by CGA, was more prominent in patients undergoing hemodialysis than in those not undergoing hemodialysis. 3 key findings →

Participants: 328 Evidence: low

Two analytical themes were identified: (1) challenges in preserving the person's voice throughout the dementia trajectory, reflecting a shift toward caregiver-mediated decision-making, assumptions about capacity, and delayed ACP initiation; and (2) challenges in maintaining continuity of expressed values and preferences over time, reflecting uncertainty about future care needs and the limitations of one-time ACP conversations. 5 key findings →

Evidence: low

Beyond “Denial”: Understanding and Responding to Help-Refusal in Dementia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-26

Evidence for interventions that reduce refusal is strongest for music during personal care and modified bathing methods, with some support for positive communication and person-centred approaches, though quality is generally low and few studies involve family caregivers in community settings. 5 key findings →

Design: narrative review Evidence: low

Short-Horizon Metrics and the Persistence of Capacity-Debiting Practices in Nursing Homes

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-13

Interventions that reduce functional capacity — antipsychotics or benzodiazepines for agitation, activity restriction for fall prevention, prolonged bed rest, incontinence product use, and catheterization — remain common in nursing homes even though functional decline is measured, publicly reported, and built into Five-Star ratings. 5 key findings →

Evidence: low

Identifying Individualized Multiple Chronic Condition Pathways Associated with Dementia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-10

Unlike traditional eager decision trees (eagerDT), which lacked sufficient training data for 17%-33% of patient profiles, lazyDT-MCCPath successfully modeled all profiles and achieved a 0.17 improvement in AUROC (0.66 vs. 0.83). lazyDT-MCCPath effectively translates pre-existing MCC profiles into personalized dementia risk probabilities for emerging conditions, which may help clinicians prioritize MCCs to monitor more closely. 1 key finding →

Evidence: low

Deep learning classifiers trained on structural magnetic resonance imaging (MRI) are increasingly proposed for early detection of Alzheimer’s disease (AD) and mild cognitive impairment (MCI), yet the pipelines that produce these models depend on shared datasets, pre-trained weights, and federated updates that an adversary can poison. 1 key finding →

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 27,380 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