Get help now — free helplines

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In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Find studies

Showing 1–25 of 59 studies in Preprints.org (page 1 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.

Exploring Natural Compounds for Alzheimer's Disease: Virtual Screening and Docking Study with KIBRA Protein

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2024-02-05

Therapies targeting amyloid, such as monoclonal antibodies like Lecanemab, Aducanumab, and Donanemab, have garnered FDA approval but remain controversial due to limited clinical benefits and significant side effects against Alzheimer. 4 key findings →

Evidence: low

Blood Plasma Coenzyme Q 10 and P-Selectin Are Predictive Factors for Mild Cognitive Dysfunction in Elderly Women

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100.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

Detection of the early phases of cognitive dysfunction is critical for identifying individuals at risk of neurodegeneration before irreversible damage occurs. 3 key findings →

Design: cross-sectional Evidence: moderate

AT(N)-Anchored Multimodal Deep Learning for Alzheimer’s Staging: A Taxonomy and Continuous Burden Index for Low-Resource Settings

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-09-25

The global burden of dementia is heavily concentrated in low- and middle-income countries (LMICs), yet biological diagnosis of Alzheimer’s Disease (AD) relies on positron emission tomography (PET) and cerebrospinal fluid (CSF) analysis that are operationally inaccessible in these regions. 5 key findings →

Evidence: low

This structural configuration shields the scaffold from calpain-mediated cleavage, reconfiguring FLNA into an active motility engine driving invasive lamellipodia but stalls proteolytic processing and forces an absolute loss of the nuclear FLNA-90 tumor-suppressor brake, unleashing uninhibited c-Myc oncogenic transcription. 5 key findings →

Evidence: low

Interpretable Frequency-Aware Deep Learning for Multi-Class EEG Classification of Neurological Disorders

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-12

Electroencephalography (EEG) records cortical activity with high temporal resolution without radiation and at low cost, which makes it a practical signal for automated screening of neurological disorders. 5 key findings →

Evidence: low

The Somnogenesis System: A Proposed Biological System for Psychiatry

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-08

For more than 150 years, since the idea that mental illness is rooted in the brain first emerged in the mid-1800s, psychiatry has searched for a reliable biological system to anchor its understanding of mental illness. 5 key findings →

Evidence: low

A Physicist's Perspective on Metabolic Rejuvenation After 50

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

Chronic metabolic diseases, including Type 2 Diabetes, hypertension, non-alcoholic fatty liver disease (NAFLD), prostate enlargement, musculoskeletal joint friction, cardiac arrhythmias, neurodegenerative waste accumulation (Alzheimer's), and elevated intraocular hydraulic pressure (glaucoma), are frequently treated as distinct, unavoidable consequences of chronological aging. 5 key findings →

Evidence: low

Alzheimer’s disease (AD) pathology is increasingly recognized to manifest in the retina, offering a non-invasive window for early biomarker discovery. 2 key findings →

Design: longitudinal study Participants: 40 Evidence: moderate

Artificial Intelligence in Alzheimer’s Disease: Evidence Maturity and Clinical Translation Across the Care Pathway

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

Artificial intelligence (AI) is now a credible translational research platform across the Alzheimer’s disease (AD) pathway, but its clinical value is often difficult to judge from performance metrics alone. 5 key findings →

Design: longitudinal study Evidence: moderate

A Biophysical Framework for Neurodegeneration: Prioritizing Protein Homeostasis Over Aggregate Toxicity

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2025-12-31

Neurodegenerative research has long hypothesized that aggregated proteins such as amyloid‑β (Aβ), tau, and α‑synuclein (αSyn) are intrinsically toxic and are directly associated with the etiologies of Alzheimer’s disease (AD) and Parkinson’s disease (PD). 1 key finding →

Evidence: low

ScFv-h3D6 Prevents Bapineuzumab-Induced Hemorrhagic Events in the APP23 Mouse Model of Alzheimer’s Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2025-11-05

The occurrence of amyloid-related imaging abnormalities (ARIA), found in clinical trials for Aβ-immunotherapy, has been related to the antibody’s effector function on glial activation by the Fc portion of the antibody. 2 key findings →

Evidence: low

Beyond Glycemic Control: The Pleiotropic Role of GLP-1RAs and Melatonin in Combating Neuroinflammation and Mitochondrial Dysfunction

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-28

Mitochondrial dysfunction, oxidative stress, neuroinflammation, and impaired protein homeostasis form interconnected pathological networks in acute central nervous system injury and chronic neurodegenerative disease. 5 key findings →

Design: narrative review Evidence: low

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have moved rapidly from metabolic medicine into neurology, but the evidence to mid-2026 refuses to resolve into a single narrative of neuroprotection. 5 key findings →

Design: clinical trial Evidence: low

EVOKE and EVOKE+ trials showed no population-level slowing of early symptomatic Alzheimer’s disease (AD) with semaglutide, motivating an assessment of whether clinical-note phenotyping over decades of routine care could identify distinct AD trajectories. 3 key findings →

Participants: 2,169 Evidence: low

Association Between Combined Multiple Behaviors and Cognitive Impairment in Older Adults: A 10-Year Cohort Study

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

Of total 8,321 participants, 24.88% (2,070) developed cognitive impairment during a 10-year follow-up. 5 key findings →

Design: longitudinal study Participants: 8,321 Evidence: moderate

Autophagy Stimulation by Intermittent Fasting and Its Potential Neuroprotective Role in Alzheimer’s Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-08-24

Alzheimer’s disease (AD) is characterised by progressive accumulation of misfolded proteins and failure of cellular clearance pathways, particularly the autophagy–lysosomal system. 2 key findings →

Evidence: high

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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