Alzheimer's disease (AD) is the most common cause of disability in individuals aged >65 years worldwide. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Since there is no effective Alzheimer's disease (AD)-modifying therapy available currently, early analysis of AD core biomarkers has become one of great significance and common concern in clinical diagnosis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Triggering receptor expressed on myeloid cells 2 (TREM2) is a member of the immunoglobulin superfamily and associates with TYRO protein tyrosine kinase-binding protein at the cell membrane to form a receptor signaling complex. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Epidemiological and experimental studies have suggested that high dietary intake of fats is associated with cognitive decline and a significantly increased risk of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Available drugs for the global Alzheimer disease (AD) epidemic only treat the symptoms without modifying disease progression. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Due to the vast differences in chemical properties among small molecule drugs, nucleotide drugs, and superparamagnetic iron oxide nanocubes (SPIONs), such as charge and hydrophobicity, entrapment of these within a single carrier for traceable synergistic therapy has been proven difficult. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a chronic neurodegenerative disease, which is considered as one of the most intractable medical problems with heavy social and economic costs. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a central degenerative disease characterized by cognitive impairment. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
Amyloid-β (Aβ) peptides accumulate in the brain and initiate a cascade of pathologic events in Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A complex composed of presenilin (PS), nicastrin, PEN-2, and APH-1 is absolutely required for γ-secretase activity in vivo. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Previous studies have led to the proposal that patients with Alzheimer's disease (AD) may have disturbed functional connectivity between different brain regions. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent functional imaging studies have indicated that the pathophysiology of Alzheimer's disease (AD) can be associated with the changes in spontaneous low-frequency (<0.08 Hz) blood oxygenation level-dependent fluctuations (LFBF) measured during a resting state. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) patients often have visual disorders which may be due to retinal nerve degenerative changes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
Synaptic loss is the cardinal feature linking neuropathology to cognitive decline in Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized pathologically by the abundance of senile plaques and neurofibrillary tangles in the brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS) is one of the most common genetic diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Capturing the systemic effects of drugs in vivo remains a fundamental challenge for drug repurposing strategies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
Full summary, score breakdown and related studies → Original source
16/100
Alzheimer’s disease (AD) is characterized by progressive memory decline, with the medial entorhinal cortex (MEC) representing an early vulnerable hub for spatial cognition. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sensitive human data underpin discoveries across medicine, biology and the social sciences, yet privacy regulation often prevents sharing them with collaborators or artificial intelligence (AI) systems. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →