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Research

27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1,101–1,125 of 1,426 studies scoring ≤ 29 out of 100 (page 45 of 58) · 27,380 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 12,859 studies have no institution on record and are not counted here.

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.

Neuroprotective potential of Acetylcholinesterase Inhibitors from Natural Sources in Combating Neurodegenerative Diseases

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. ScienceOpen Preprints 2026-09-08

Neurodegenerative diseases comprise a diverse group of progressive disorders characterized by the selective and irreversible loss of neuronal structure and function within the specific regions of the central and/or peripheral nervous systems. 5 key findings →

Design: narrative review Evidence: low

Full summary, score breakdown and related studies → Original source

Multi-Omics Analysis Reveals Molecular Responses of Alkaloid Content Variations in Lycoris radiata Across Different Locations

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-09-08

The Amaryllidaceae geophyte Lycoris radiata is a primary botanical source of high-value medicinal alkaloids, including the Alzheimer’s therapeutic galanthamine. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Bee Venom-Loaded Nanoliposomes as an Antioxidant and Erythroprotective Delivery Platform for In Vitro Controlled Release and Improved Gastrointestinal Stability

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-09-07

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

Full summary, score breakdown and related studies → Original source

Transthyretin Contributes to Hippocampal Blood-Brain Barrier Recovery Following Intestinal Inflammation, with Reduced Expression in Alzheimer’s Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-04

These findings identify TTR as a contributor of adaptive neurovascular homeostasis during gut-derived neuroinflammation. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Gut community-level analysis reveals an altered balance between Phocaeicola vulgatus and Bacteroides fragilis in Alzheimer’s disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-08-13

Gut microbiome differences in Alzheimer’s disease (AD) are typically cataloged taxon by taxon, yet bacterial competition and cross-feeding make species’ roles dependent on the entire community. 1 key finding →

Participants: 274 Evidence: moderate

Full summary, score breakdown and related studies → Original source

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

Full summary, score breakdown and related studies → Original source

Gut microbiota mediates the association between aging and cognitive function: evidence from a population-based Kyotango study linking diet, Bifidobacterium, and Mini-Mental State Examination (MMSE) score

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-08-04

Our findings provide evidence that age-related changes in the gut microbiota, particularly reductions in Bifidobacterium , partially mediate cognitive decline in older adults. 5 key findings →

Design: cross-sectional Participants: 578 Evidence: low

Full summary, score breakdown and related studies → Original source

Precision Nanocrystal Theranostics for Neurodegenerative Proteopathies: Strategies to Cross the Blood-Brain Barrier and Target Protein Aggregation

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

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

Full summary, score breakdown and related studies → Original source

Depth-Dependent Alterations in Cerebral Blood and Tissue Oxygenation Associated with Tau in Alzheimer’s Disease Models

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

Vascular dysfunction is increasingly recognized as a feature of Alzheimer’s disease (AD), and inadequate oxygen delivery may contribute to neuronal death. 5 key findings →

Design: longitudinal study Evidence: moderate

Full summary, score breakdown and related studies → Original source

Upper cervical spinal cord morphometric charts: from population references to individualized clinical assessment

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

The upper cervical spinal cord is essential for motor, sensory and autonomic function, yet its normative morphometric trajectories and disease-related deviations remain unclear. 2 key findings →

Participants: 2,394 Evidence: low

Full summary, score breakdown and related studies → Original source

Carbonic anhydrase inhibition rescues heart function in the Tg2576 Alzheimer’s mouse model by ameliorating cardiac amyloid-β pathology and neurotrophic-signaling impairment

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-09

FDA-approved carbonic anhydrase inhibitors (CAIs) have shown robust efficacy in reducing amyloid-β (Aβ) pathology, neurodegeneration, and cerebrovascular dysfunction in Alzheimer’s disease (AD) and cerebral amyloid angiopathy (CAA) models, highlighting carbonic anhydrase (CAs) as a promising, previously untapped therapeutic target for AD and vascular contribution to dementia. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Spermine inhibits ferroptosis in vascular dementia rats by intervening Nrf2/SLC7A11/GPX4 expression in chondriosome

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-09

Spermine exerts neuroprotective effects in VaD by inhibiting TRPM2-mediated oxidative stress and activating the Nrf2/SLC7A11/GPX4 pathway, thereby suppressing ferroptosis. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Generalizing Amyloid β Pathology from Postmortem Human Brains with Vision Foundation Models for Lesion Quantification

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-07

The ViTamyloid classifier achieved strong feature-separation metrics, yielding area under the receiver operating characteristic curve (AUROC) and precision-recall curve (AUPRC) values of 0.994/0.958 for CCP, 0.989/0.945 for CGP, 0.992/0.977 for CAA Type 1, and 0.997/0.978 for CAA Type 2. 4 key findings →

Design: longitudinal study Evidence: moderate

Full summary, score breakdown and related studies → Original source

Disease stage-sensitive MFSD2A-caveolae axis insigates hippocampal blood–brain barrier disruption in Alzheimer’s disease

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

Blood-brain barrier (BBB) malfunction contributes to pathophysiology of Alzheimer’s disease (AD), yet the mechanisms that confer hippocampal endotheliocytes vulnerability remain unclear. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Contribution of cerebrovascular lesions to neurodegeneration and cognitive decline

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-06

Vascular risk factors were associated with CSVD burden and progression, and WMH and PVS progression were further associated with cortical atrophy and cognitive decline, underscoring the interconnected contributions of vascular risk, CSVD, and neurodegeneration to cognitive aging and dementia risk. 5 key findings →

Design: cross-sectional Participants: 289 Evidence: moderate

Full summary, score breakdown and related studies → Original source

APOE4 reduction in vascular-associated fibroblasts decreases cerebral amyloid angiopathy and associated vascular dysfunction

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-04

Cerebral amyloid angiopathy (CAA), characterized by cerebrovascular amyloid deposition, is strongly associated with Alzheimer’s disease, ischemic injury, and lobar hemorrhages. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

The Alzheimer’s Disease-associated gene CD2AP regulates permeability of endothelial cells and transendothelial migration of immune cells

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-02

Variants at the CD2AP locus, which encodes a branched-actin regulator, are associated with late-onset Alzheimer’s disease (AD), and CD2AP-deficient mice show increased blood-brain barrier (BBB) permeability. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Neurodegeneration-inducing macromolecules exit the brain via nanovascular conduits formed by reticular fibroblasts

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-27

Accumulation of proteins such as amyloid β (Aβ), hyperphosphorylated tau and α-synuclein within the brain alters neural information processing and causes neurodegeneration 1–3 , but how toxic solutes are cleared from the brain remains highly controversial 4,5 . 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Inflammatory biomarker candidates in dementia with Lewy bodies: diagnostic classification, clinical associations, and survival

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-11-01

Dementia with Lewy bodies (DLB) is a common neurodegenerative dementia that remains difficult to distinguish clinically from Alzheimer's disease (AD) and related disorders because of overlapping clinical features and frequent mixed pathology. 4 key findings →

Participants: 20 Evidence: low

Full summary, score breakdown and related studies → Original source

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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