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

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 18,501–18,525 of 27,146 studies marked Peer-reviewed (page 741 of 1086) · 28,180 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; 13,658 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.

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

Chronic caffeine consumption prevents obesity-induced cognitive and memory impairments by reducing neuroinflammation and enhancing neuronal activity in the hippocampus

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Pharmacological Research 2026-02-13

Obesity and its associated metabolic disturbances increase the risk of cognitive decline, dementia, and anxiety-related disorders. 2 key findings →

Evidence: low

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

Molecular Crossroads: Shared and Divergent Molecular Signatures in Alzheimer’s Disease and Dementia with Lewy Bodies

✓ Peer-reviewed alzhub usefulness score 41 out of 100. International Journal of Molecular Sciences 2025-12-07

Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) are the two most common forms of dementia due to neurodegeneration. 5 key findings →

Evidence: low

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

Intercellular signaling and synaptic deconstruction uncovered by single-cell and spatial transcriptomics in an AD tauopathy model

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Communications Biology 2025-11-17

Alzheimer’s disease (AD) is the leading cause of dementia in elderly individuals worldwide; however, all mechanisms leading to disease onset and progression are not well understood. 3 key findings →

Evidence: low

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

Seeding biosensor cell line that reproduces the Alzheimer tau fold

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Biological Chemistry 2025-11-20

The assembly of tau protein into amyloid filaments through templated seeding is believed to underlie the propagation of pathology in neurodegenerative diseases, such as Alzheimer's disease (AD) and other tauopathies. 1 key finding →

Evidence: low

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

Selective association of EEG microstates with clinical symptoms and mutation status in monogenic Alzheimer disease

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

• EEG microstate analyses were performed in a cohort of autosomal dominant AD. • Coverage of class C decreased in symptomatic mutation carriers • Coverage of class D decreased in presymptomatic and symptomatic mutation carriers. • Coverage of class E increased in presymptomatic and symptomatic mutation carriers. • The findings may support presymptomatic changes in resting-state neuronal networks. 4 key findings →

Participants: 99 Evidence: moderate

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

Effects of Heparan Sulfate Trisaccharide Containing Oleanolic Acid in Attenuating Hyperphosphorylated Tau-Induced Cell Dysfunction Associated with Alzheimer’s Disease

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Medicinal Chemistry 2025-01-22

Alzheimer's disease (AD) is the most common form of dementia, marked by progressive brain degeneration and cognitive decline. 2 key findings →

Evidence: low

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

In Vitro and In Vivo Evaluation of Small-Molecule Disassemblers of Pathological Tau Fibrils

✓ Peer-reviewed alzhub usefulness score 41 out of 100. ACS Chemical Neuroscience 2026-01-05

Aggregation of the microtubule-binding protein tau is the histopathological hallmark of Alzheimer's disease (AD) and other neurodegenerative diseases, which are collectively known as tauopathies. 5 key findings →

Evidence: low

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

↑ 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 (3.7% 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