alzhub.org
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.

Research

28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 7,426–7,450 of 15,839 studies scoring 30–49 out of 100 (page 298 of 634) · 28,580 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; 14,058 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.

Cardiovascular-kidney-metabolic syndrome, systemic inflammation, and incident dementia: evidence from 400,740 UK Biobank participants

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Diabetology & Metabolic Syndrome 2025-07-03

Compared with stage 0 CKM syndrome, stages 3 and 4 were significantly associated with an increased risk of dementia (hazard ratio [HR], 1.35; 95% confidence interval [CI], 1.14-1.59; HR, 1.80; 95% CI 1.57-2.07). 5 key findings →

Participants: 389,287 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Association of sugar intake with incident dementia in the UK Biobank: a prospective cohort study

✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of Prevention of Alzheimer s Disease 2025-08-05

Higher intakes of total sugar (HR = 1.292, 95 % CI = 1.148--1.453) and free sugar intake (HR = 1.254, 95 % CI = 1.117--1.408) were significantly associated with increased dementia risk. 4 key findings →

Participants: 172,516 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

UK Biobank MRI data can power the development of generalizable brain clocks: A study of standard ML/DL methodologies and performance analysis on external databases

✓ Peer-reviewed alzhub usefulness score 41 out of 100. NeuroImage 2025-01-30

In this study, we present a comprehensive pipeline to train and compare a broad spectrum of machine learning and deep learning brain clocks, integrating diverse preprocessing strategies and correction terms. 1 key finding →

Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Proteomics of the temporal cortex in semantic dementia reveals brain-region specific molecular pathology and regulation of the TDP-43-ANXA11 interactome

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Acta Neuropathologica Communications 2025-07-25

Semantic dementia (SD) is a clinical subtype of frontotemporal dementia characterized by impaired word comprehension and semantic memory, and occurs nearly always sporadically. 1 key finding →

Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Myopathic aggregation-prone variants in the TDP-43 prion-like domain: genetics paving the way

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Brain 2025-02-26

While neuropathological and genetic studies have established the crucial involvement of TDP-43 proteinopathy in the pathogenesis of amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and related neurodegenerative disorders, multiple studies have described the presence of TDP-43 inclusions in muscular disorders, including inclusion body myositis but also other related rimmed vacuole myopathies. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Defining the Intestinal eCBome and Oxylipin Signaling Systems in a TDP‐43 Mouse Model of Frontotemporal Dementia

✓ Peer-reviewed alzhub usefulness score 41 out of 100. The FASEB Journal 2026-01-12

Frontotemporal dementia (FTD) is a group of early onset and progressive disorders, characterized by degeneration in the frontal and temporal lobes, and subsequent deterioration in cognition, personality, social behavior, and language, with aggregates of the RNA-binding protein TDP-43 being present in ~45% of the cases. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

RNA-binding proteins TDP-43 and FUS promote R-loop resolution and regulate transcription termination

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Biological Chemistry 2026-03-06

TDP-43 and FUS are RNA-binding proteins involved in the regulation of diverse RNA-processing events and have been strongly implicated in neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Data‐driven discovery of midlife cardiometabolic profile associated with incident early‐onset and late‐onset dementia

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Diabetes Obesity and Metabolism 2025-03-06

During a median follow-up of 14.1 years, 279 early-onset dementia cases and 3167 late-onset dementia cases were documented. 5 key findings →

Participants: 249 Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Semaglutide improves cognitive function and neuroinflammation in APP/PS1 transgenic mice by activating AMPK and inhibiting TLR4/NF-κB pathway

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Alzheimer s Disease 2025-03-28

BackgroundAlzheimer's disease (AD) causes cognitive function disorder and has become the preeminent cause of dementia. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Longan Aril polysaccharides ameliorate cognitive impairment in AD mice via restoration of the immune phagocytosis of microglia

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Ethnopharmacology 2025-02-07

LAPs contained five monosaccharides. LAPs improved cognitive function and increased the number of Nissl bodies, lactate secretion, the IL-10 content, the relative fluorescence intensity of the IBA1 and AXL proteins, and the protein expression levels of AXL, Mertk, Glut1, HK2, PI3K, p-Akt/Akt, p-mTOR/mTOR and HIF-1α of immune-tolerant AD mice. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Neuroprotective effects of SGLT2 inhibitors empagliflozin and dapagliflozin on Aβ 1–42 -induced neurotoxicity and neuroinflammation in cellular models of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Alzheimer s Disease 2025-03-20

SGLT2i empagliflozin and dapagliflozin exhibited neuroprotective actions against human Aβ 1–42 -induced neurotoxicity. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Rescue of protein dyshomeostasis in hippocampal astrocytes from an Alzheimer’s disease mouse model by stabilizing ER-mitochondrial interactions at a 20 nm distance

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Alzheimer s Research & Therapy 2025-07-04

Autophagic markers beclin 1, LC3II and p62, and lysosome-related marker cathepsin B, all upregulated in AD astrocytes, were significantly reduced, while autophagic flux was rescued, by stabilizing 20 nm-MERCS. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

UCH-L1 in Alzheimer’s Disease: A Crucial Player in Dementia-Associated Mechanisms

✓ Peer-reviewed alzhub usefulness score 41 out of 100. International Journal of Molecular Sciences 2025-09-16

Ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1) is a critical deubiquitinating enzyme that is highly expressed in the central nervous system, where it participates in protein degradation and turnover as part of the ubiquitin-proteasome system (UPS). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Targeting NLRP3 signaling with a novel sulfonylurea compound for the treatment of vascular cognitive impairment and dementia

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Fluids and Barriers of the CNS 2025-06-03

AMS-17 treatment improved cognitive function, enhanced blood-brain barrier (BBB) integrity, and promoted remyelination in VaD mice. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Neuroinflammation in vascular cognitive impairment and dementia: Insights from clinical biomarkers and experimental models

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Cerebral Blood Flow & Metabolism 2026-04-10

Vascular cognitive impairment and dementia (VCID) encompasses a heterogeneous group of disorders in which cerebrovascular pathology contributes to cognitive decline. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Assessing the Roles of Aging, Estrogen, Nutrition, and Neuroinflammation in Women and Their Involvement in Alzheimer’s Disease—A Narrative Overview

✓ Peer-reviewed alzhub usefulness score 41 out of 100. International Journal of Molecular Sciences 2026-01-26

The purpose of this narrative review is to examine women's cognitive health and to highlight its association with four major pillars: (1) aging, (2) estrogen decline and loss, (3) diet, and (4) neuroinflammation, and their contribution to cognitive decline, with a focus on this combination to increase awareness and address the progression and potential amelioration of Alzheimer's disease (AD). 2 key findings →

Design: narrative review Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Microglial histone H3K18 crotonylation promotes STAT1 expression and induces cognitive deficit in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Frontiers in Immunology 2026-01-27

Hippocampal pan-histone H3 crotonylation (H3Kcr) and H3K18cr were significantly upregulated in both 5xFAD and Aβ42-injected mice compared to controls. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

↑ 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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.

1,034 records (3.6% 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