Dementia is a rapidly rising global health crisis that silently disables families and ends lives and livelihoods around the world. 4 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.
Neurodegenerative disorders such as Alzheimer's disease (AD), the most common form of dementia, represent a growing global health crisis, yet current treatment strategies remain primarily palliative. 2 key findings →
Design: longitudinal study Evidence: moderate
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Four clones were isolated from an adult human brain complementary DNA library with an oligonucleotide probe corresponding to the first 20 amino acids of the beta peptide of brain amyloid from Alzheimer's disease.
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56/100
An amyloid protein that precipitates in the cerebral vessel walls of Dutch patients with hereditary cerebral hemorrhage with amyloidosis is similar to the amyloid protein in vessel walls and senile plaques in brains of patients with Alzheimer's disease, Down syndrome, and sporadic cerebral amyloid angiopathy.
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Amyloid PET and sleep duration information was acquired on 4425 cognitively unimpaired participants (mean [SD] age, 71.3 [4.7] years; 2628 [59.4%] female; 1509 [34.1%] tested Aβ positive). 4 key findings →
Design: cross-sectional Evidence: low
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Neurotoxic amyloid beta peptide (Abeta) accumulates in the brains of individuals with Alzheimer disease (AD). 2 key findings →
Evidence: low
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Epidemiological studies suggest that increased intake of the omega-3 (n-3) polyunsaturated fatty acid (PUFA) docosahexaenoic acid (DHA) is associated with reduced risk of Alzheimer's disease (AD). 5 key findings →
Evidence: low
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After 1 year, 8 of 37 patients with MCI converted to AD (22%). 3 key findings →
Participants: 37 Evidence: low
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55/100
The brain changes associated with AD may already begin developing early in middle age, especially among APOE epsilon 4 carriers. 5 key findings →
Participants: 603 Evidence: low
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In this large, population-based cohort, baseline and long-term average serum total cholesterol levels were not associated with the risk for incident AD. 3 key findings →
Participants: 1,026 Evidence: moderate
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Even when adjusted for age at onset, symptom duration, and other demographic variables, APOEε2 is associated with milder AD pathology and less severe antemortem cognitive impairment compared to APOEε3 and ε4 alleles, suggesting a relative neuroprotective effect of APOEε2 in AD. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
55/100
Low CSF Abeta(1-42) (surrogate for Abeta amyloid load) is more closely linked to the presence of APOE epsilon4 than to clinical status. 3 key findings →
Participants: 399 Evidence: low
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CST3 is a susceptibility gene for late-onset AD, especially in patients aged 75 years and older. 2 key findings →
Design: case-control study Participants: 260 Evidence: moderate
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Subjects included 96 males and 118 females with a mean age at death of 86 years (SD, 7). 1 key finding →
Design: longitudinal study Participants: 96 Evidence: moderate
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55/100
Amyloid-positive cognitively healthy participants showed a significant increase in mI/creatine and mI/NAA levels compared to amyloid-negative healthy elderly (p Conclusions mI levels are elevated already at asymptomatic stages of AD. 2 key findings →
Design: cross-sectional Evidence: low
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Of 102 607 individuals in the study, 56 559 (55%) were women (median age, 58 years [IQR, 47-67 years]). 5 key findings →
Participants: 607 Evidence: high
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Reliable blood biomarkers for Alzheimer's disease (AD) are missing. 1 key finding →
Participants: 28 Evidence: low
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The strong correlation between hippocampal atrophy and beta-amyloid (Abeta) burden in the Pittsburgh compound B-positive healthy control group suggests that Abeta deposition in the inferior temporal neocortex is related to hippocampal synaptic and neuronal degeneration. 3 key findings →
Participants: 32 Evidence: low
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Apolipoprotein E (APO-E) binds to the beta-amyloid peptide and is present in senile neuritic plaques in Alzheimer's disease (AD). 2 key findings →
Evidence: low
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The results suggest that APOE epsilon4 and heavy drinking and heavy smoking lower the age of onset for AD in an additive fashion. 2 key findings →
Design: cross-sectional Participants: 397 Evidence: moderate
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Exposure to particulate matter (PM) in the ambient air and its interactions with APOE alleles may contribute to the acceleration of brain aging and the pathogenesis of Alzheimer's disease (AD). 1 key finding →
Evidence: moderate
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Our results indicate that the inflammatory properties of circulating neutrophils shift as the percentage of aged neutrophils expands in patients with AD-changes that may play an instrumental role in establishing systemic chronic inflammation. 3 key findings →
Participants: 42 Evidence: low
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The defining features of Alzheimer disease (AD) include conspicuous changes in both brain histology and behavior. 4 key findings →
Evidence: low
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One hallmark of Alzheimer disease is the accumulation of amyloid beta-peptide in the brain and its deposition as plaques. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) results in cognitive decline and altered network activity, but the mechanisms are unknown. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
10 of the 1,610 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.
- (11)C-PBR28 binding to translocator protein increases with progression of Alzheimer's disease
- Amyloid precursor protein revisited: neuron-specific expression and highly stable nature of soluble derivatives
- Cerebral metabolic and cognitive decline in persons at genetic risk for Alzheimer's disease
- Advanced glycation end products contribute to amyloidosis in Alzheimer disease
- Knock-in models related to Alzheimer's disease: synaptic transmission, plaques and the role of microglia
- Sex-specific effects of apolipoprotein E ε4 genotype on longitudinal hippocampal atrophy in amnestic mild cognitive impairment over a 2-year evaluation period
- Melatonin in Alzheimer's Disease: A Latent Endogenous Regulator of Neurogenesis to Mitigate Alzheimer's Neuropathology
- Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer's Disease
- Shifts in gut microbiota composition in an APP/PSS1 transgenic mouse model of Alzheimer's disease during lifespan
- Selective association of EEG microstates with clinical symptoms and mutation status in monogenic Alzheimer disease
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 →