Based on the reduction of amyloid β plaques, US FDA has recently approved Aducanumab as a disease modifying treatment for Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) is a neurological condition that affects millions of individuals around the world and for which there are few effective therapies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
The Apolipoprotein E ε4 (ApoE ε4) allele, encoding ApoE4, is the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Human apolipoprotein E (ApoE) is a 299-amino acid secreted glycoprotein that binds cholesterol and phospholipids. 1 key finding →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
The central role of the resident innate immune cells of the brain (microglia) in neurodegeneration has become clear over the past few years largely through genome-wide association studies (GWAS), and has rapidly become an active area of research. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cancer continues to be a substantial health concern and a leading cause of death in the United States and around the world. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The receptor Triggering Receptor Expressed on Myeloid cells 2 (TREM2) is associated with several neurodegenerative diseases including Alzheimer's Disease and TREM2 stimulation represents a novel therapeutic opportunity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Autosomal dominant Alzheimer's disease (ADAD) is a rare early-onset form of Alzheimer's disease, caused by dominant mutations in one of three genes: presenilin 1, presenilin 2, and amyloid β precursor protein (APP). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The gene regulatory network analysis identified several hub genes regulated in AD, PD, and MS, in which HSPB1 and HSPA1A were key molecules. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Over the past 30 years, the majority of (pre)clinical efforts to find an effective therapy for Alzheimer's disease (AD) focused on clearing the β-amyloid peptide (Aβ) from the brain since, according to the amyloid cascade hypothesis, the peptide was (and it is still considered by many) the pathogenic determinant of this neurodegenerative disorder. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
On July 6, 2023, the U.S. Food and Drug Administration (FDA) approved lecanemab (Leqembi) for the treatment of Alzheimer's dementia (AD) patients. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Alzheimer's Disease (AD) is a leading cause of morbidity. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) has witnessed a gradual rise in its prevalence in recent decades, particularly impacting a substantial segment of individuals aged 85 and above. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The results from the gantenerumab phase 3 programs are expected by the end of 2022 and will add critical information to the collective knowledge on the search for effective AD treatments. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Lecanemab, an anti-amyloid antibody with effects on biomarker and clinical endpoints in early Alzheimer's Disease (AD), was granted accelerated approval by the FDA in 2023 and regulatory review in Europe is ongoing. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia affecting millions of individuals, including family members who often take on the role as caregiver. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
After the CLARITY-AD clinical trial results of lecanemab were interpreted as positive, and supporting the amyloid hypothesis, the drug received accelerated Food and Drug Administration approval. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research on disease-modifying treatments for Alzheimer's disease has resulted in a series of failures over the past 20 years. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Clinicians specialized in the diagnosis and management of persons living with early-stage Alzheimer's disease need to enable access, for those meeting criteria, to the new class of disease modifying drugs (DMDs). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies are heterogeneous clinicopathological entities characterized by abnormal neuronal and/or glial inclusions of the microtubule-binding protein tau. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A mouse model of tauopathy and human myocardial and brain tissue from patients with HF, AD, and controls was employed in this study. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
With the failure of various amyloid-β-targeted drugs for Alzheimer's disease (AD) in clinical trials, tau protein has gained growing attention as an alternative therapeutic target in recent years. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies are clinicopathological entities with increased and pathological deposition in glia and/or neurons of hyperphosphorylated aggregates of the microtubule-binding protein tau. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau protein is a key target of interest in developing therapeutics for neurodegenerative diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a form of dementia characterized by progressive memory decline and cognitive dysfunction. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 3,106 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Reducing placebo response in clinical trials of agitation in Alzheimer’s disease
- Combining billing codes, clinical notes, and medications from electronic health records provides superior phenotyping performance
- Inhibition of GSK-3 ameliorates Abeta pathology in an adult-onset Drosophila model of Alzheimer's disease
- Treatment with a copper-zinc chelator markedly and rapidly inhibits beta-amyloid accumulation in Alzheimer's disease transgenic mice
- Vasomechanic treatment increases efflux of human brain proteins
- Association between Statin Use and Sepsis Risk in Patients with Dementia: A Retrospective Cohort Study
- [Toward a preventive management Alzheimer's disease]
- Behavioral symptoms in Alzheimer's disease: phenomenology and treatment
- Screening for cognitive impairment in older adults: A systematic review for the U.S. Preventive Services Task Force
- Density of GFAP-immunoreactive astrocytes is decreased in left hippocampi in major depressive disorder
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 →