Alzheimer disease (AD) is a major cause of dementia. 4 key findings →
Evidence: low
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Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Late Onset Alzheimer Disease (LOAD) constitutes the majority of AD cases (∼90%). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In an attempt to elucidate the pathological implications of intracellular accumulation of the amyloid precursor protein (APP) in postmitotic neurons in vivo, we transferred APP695 cDNA into rat hippocampal neurons by using a replication-defective adenovirus vector. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
One of the key classical pathological features of Alzheimer's disease (AD) is the progressive accumulation of amyloid beta (Aβ42) peptides and their coalescence into highly insoluble senile plaque cores. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The presence of concomitant Alzheimer pathology has been linked to earlier death in cases with dementia with Lewy bodies (DLB). 4 key findings →
Evidence: low
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Previous studies have shown that exposure to inhaled anesthetics can cause cognitive dysfunction, suggesting that general anesthesia might be a risk factor for the development of Alzheimer disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CSF biomarker studies were performed in 6 patients each with tremor-dominant (TD) and non-tremor-dominant (NT) Parkinson disease (PD) patients, 27 Alzheimer disease (AD) and 17 age-matched controls. 2 key findings →
Evidence: moderate
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Neurosyphilis is a neurological disease that involves infection of the central nervous system with Treponema pallidum. 4 key findings →
Participants: 44 Evidence: low
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Autoimmune encephalitis (AE) is a potentially treatable cause of rapidly progressive dementia that may mimic Creutzfeldt-Jakob disease (CJD). 4 key findings →
Evidence: low
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A 2-dimensional high-throughput screening method is presented to select peptide sequences from large peptide libraries for precision formulation additives, having a high capacity to specifically host a drug of interest and provide tailored drug release properties. 4 key findings →
Evidence: low
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36/100
Although Alzheimer disease (AD) remains a clinical diagnosis, biomarkers are in use to support the diagnosis. 4 key findings →
Participants: 205 Evidence: low
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Diagnosing Atypical Parkinsonian Syndromes (APS) may be challenging due to overlapping clinical features of Parkinson's disease (PD), and the lack of pathognomonic diagnostic tests. 4 key findings →
Design: narrative review Evidence: low
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Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) levels in the cerebrospinal fluid (CSF) have been associated with Alzheimer disease (AD) status. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
BackgroundAlzheimer's disease (AD) is the most prevalent neurodegenerative disorder characterized by cognitive deficit and pathological accumulation of amyloid-β (Aβ) and tau proteins. 4 key findings →
Evidence: low
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Tau phosphorylation and aggregation is the final common pathway for neuronal toxicity across multiple neurodegenerative diseases including Alzheimer disease, progressive supranuclear palsy, and corticobasal degeneration. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this study, we investigated the effects of chronic administration of an inhibitor of the β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) on Alzheimer-related pathology by multitracer PET imaging in transgenic APPPS1-21 (TG) mice. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid-β (Aβ) aggregated forms are highly associated with the onset of Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Alzheimer Disease (AD) constitutes a major global healthcare problem. 4 key findings →
Evidence: low
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An increasing number of individuals in our population are surviving to over 90 years and a subset is at risk for developing dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Disease-onset time (DOT) and disease trajectory concepts were applied to derive an Alzheimer's disease (AD) progression population model using the clinical dementia rating scale-sum of boxes (CDR-SOB) from the AD neuroimaging initiative (ADNI) database. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The amyloid hypothesis (AH) of Alzheimer's disease (AD) posits that the fundamental cause of AD is the accumulation of the peptide amyloid beta (Aβ) in the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Astrocytes are the most numerous cell type in the brain, and their physiological roles are essential for normal brain function. 4 key findings →
Evidence: low
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Residing in neighborhoods characterized by low-income, low-vehicle access, and higher low-fat milk prices was associated with a greater risk of incident dementia. 3 key findings →
Participants: 6,551 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We report that pan-neuronal expression of each ApoE allele induces lipid accumulation specifically in the brain, but not in the muscle. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Processed meats are a significant source of proteins, indispensable amino acids (IAA), A and B vitamins, zinc, phosphorus, iron, and several micronutrients (Table 1). 1 key finding →
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 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 →