Neighborhood disadvantage in later life is associated with poorer cognition and increased vulnerability to dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Lecanemab is a humanized IgG1 monoclonal antibody binding with high affinity to protofibrils of amyloid-beta (Aβ) protein. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Here the current and emerging roles of brain positron emission tomography (PET) in Alzheimer's disease (AD) in the era of anti-amyloid-β antibody therapy, with a focus on clinical applications, methodological considerations, and future perspectives were reviewed. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent advances in Blood-Based Biomarkers (BBMs) are transforming the diagnostic landscape of Alzheimer Disease (AD), with plasma p-tau217 emerging as a highly accurate and scalable diagnostic marker of AD pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
P. gingivalis-induced periodontitis dampened hippocampal Bmal1 rhythms, lowered p-AKT, activated glia, and elevated Aβ and interleukin 1β (IL-1β). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A doença de Alzheimer (DA) é uma enfermidade neurodegenerativa progressiva cuja fisiopatologia envolve, entre outros mecanismos, o acúmulo cerebral de β-amiloide, associado a alterações da proteína tau, sua hiperfosforilação e formação de emaranhados neurofibrilares, contribuindo para a disfunção sináptica e a perda neuronal. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
36/100
Epidemiological evidence suggests an association between celiac disease (CeD) and Alzheimer disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Type 2 diabetes (T2D) and dementia frequently co-occur, yet the biological mechanisms underlying this comorbidity remain incompletely understood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Lecanemab reduced clinical decline by roughly 27% over placebo, with ARIA-E in 12.6% of treated patients;donanemab slowed decline by about 35%, with ARIA-E near 24%. 4 key findings →
Design: narrative review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
-glycans found at the N304 site of lecanemab of the heavy chain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) affects ~55 million people globally and is projected to rise steeply with population ageing. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
TDP-43 proteinopathies encompass frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP), amyotrophic lateral sclerosis (ALS-TDP), and limbic predominant age related TDP-43 encephalopathy neuropathological change (LATE-NC). 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
36/100
The psychometric properties of the Neuropsychiatry Unit Cognitive Assessment short-form versions were comparable with the original, with all maintaining high convergent validity and reliability. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
To investigate alterations in resting-state electroencephalogram (EEG) microstates across the cognitive spectrum of Parkinson's disease (PD) and to evaluate their utility as electrophysiological biomarkers of cognitive impairment. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
36/100
Blood-based biomarkers are increasingly used to triage patients for amyloid confirmation, yet performance is often reported versus a single comparator despite discordance between amyloid PET and CSF. 1 key finding →
Design: cross-sectional Participants: 320 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
36/100
China has the world's highest dementia prevalence, disproportionately impacting rural areas. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Foundation models (FMs) are entering Alzheimer's disease and related dementias (ADRD), yet bedside impact remains limited. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Accurate and reproducible electroencephalography (EEG)-based classification of dementia remains a key challenge in computational neurodiagnostics. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The analyses supported stage-dependent remodeling of astrocyte-associated transcriptional and metabolic programs during disease progression. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Event-related potentials (ERPs), particularly the P300 component, provide a noninvasive, cost-effective approach to probing neural dysfunction in Alzheimer's disease (AD) and mild cognitive impairment (MCI). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Comparison of proteins between the three groups revealed significantly lower Aβ1-42, higher Tau and pTau protein expression in serum of patients with Alzheimer disease as compared to patients with mild cognitive impairment and controls. 4 key findings →
Participants: 96 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Compared with no testing, the CSF strategy yielded 0.011 additional life-years and 0.019 additional QALYs for an extra cost of THB2,589 (USD71), resulting in an ICER of THB132,961 (USD3,632) per QALY. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
36/100
Objetivo:Analisar criticamente o potencial dos exossomos sanguíneos associados a marcadores inflamatórios e ferramentas nanotecnológicas como biomarcadores hematológicos no diagnóstico precoce da Doença de Alzheimer (DA), enfatizando aplicações translacionais. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The cytoplasmic accumulation of TDP-43 aggregates remains a persistent pathological hallmark of neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and limbic-predominant age-related TDP-43 encephalopathy (LATE). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
= 7.1 nM) and remarkable selectivity over other proteinopathies. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →