Lysosome dysfunction arises early and propels Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Amyloid beta (Abeta) immunoreactivity in neurons was examined in brains of 32 control subjects, 31 people with Down syndrome, and 36 patients with sporadic Alzheimer's disease to determine if intraneuronal Abeta immunoreactivity is an early manifestation of Alzheimer-type pathology leading to fibrillar plaque formation and/or neurofibrillary degeneration. 4 key findings →
Participants: 31 Evidence: low
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Extracellular deposition of the beta/A4 amyloid peptide is a characteristic feature of the brain in patients with Alzheimer disease. beta/A4 amyloid is derived from the amyloid precursor protein (APP), an integral membrane protein that exists as three major isoforms (APP695, APP751, and APP770). 4 key findings →
Evidence: low
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Familial Danish dementia (FDD), also known as heredopathia ophthalmo-oto-encephalica, is an autosomal dominant disorder characterized by cataracts, deafness, progressive ataxia, and dementia. 4 key findings →
Evidence: low
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A significant ADI × dementia interaction was observed for global atrophy (p = .005) and several other outcomes. 5 key findings →
Design: longitudinal study Participants: 14 Evidence: moderate
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Normative developmental equations provide reliable descriptors of brain electrical activity in people 6 to 90 years old. 5 key findings →
Evidence: low
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Endocytic dysfunction is an early pathological change in Alzheimer's disease (AD) and Down's syndrome (DS). 3 key findings →
Evidence: low
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49/100
A major feature of Alzheimer's disease (AD) is the loss of noradrenergic locus coeruleus (LC) projection neurons that mediate attention, memory, and arousal. 5 key findings →
Evidence: low
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To analyze the relationship between the deposition of amyloid beta peptides (Abeta) and neuronal loss in transgenic models of Alzheimer's disease (AD), we examined the frontal neocortex (Fc) and CA1 portion of hippocampus (CA1) in PSAPP mice doubly expressing AD-associated mutant presenilin 1 (PS1) and Swedish-type mutant beta amyloid precursor protein (APPsw) by morphometry of Abeta burden and neuronal counts. 4 key findings →
Evidence: low
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In cerebral amyloid angiopathy (CAA), amyloid fibrils deposit in walls of arteries, arterioles and less frequently in veins and capillaries of the central nervous system, often resulting in secondary degenerative vascular changes. 3 key findings →
Evidence: low
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By 2060, ADRD cases in China are projected to reach approximately 49.89 million, with the highest prevalence and economic burden concentrated in provinces such as Shandong, Sichuan, Jiangsu, Henan, and Guangdong. 5 key findings →
Design: longitudinal study Evidence: moderate
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Study objectives Emerging evidence suggests a role for sleep in contributing to the progression of Alzheimer disease (AD). 3 key findings →
Evidence: low
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The QDRS provides a rapid method to determine study eligibility; stage patients in clinical practice; and improve case ascertainment in population studies. 2 key findings →
Evidence: low
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Study of the hippocampal formation of 82 subjects, including 25 control subjects from 33 to 83 years of age, 34 subjects with Alzheimer disease (AD) from 65 to 89 years of age, and 23 subjects with Down syndrome (DS) from 33 to 72 years of age, revealed hippocampal vasculopathy with fibrosis and calcification (VFC) in 40% of control, 59% of AD, and 4% of DS subjects. 5 key findings →
Participants: 82 Evidence: moderate
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Immunotherapies for various neurodegenerative diseases have recently emerged as a promising approach for clearing pathological protein conformers in these disorders. 5 key findings →
Evidence: low
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These data support the hypothesis that neuronal endosomal dysfunction is associated with preclinical AD. 4 key findings →
Evidence: low
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Evidence suggests that Alzheimer disease (AD) begins as a disorder of synaptic function, caused in part by increased levels of amyloid beta-peptide 1-42 (Abeta42). 4 key findings →
Evidence: low
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Increasing evidence points to synaptic plasticity impairment as one of the first events in Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Older age was associated with greater odds of abnormal p-Tau217 (odds ratio [OR] 1.08 per year, 95% CI 1.07–1.09), as was APOE ε4 carrier status (OR 3.32, 95% CI 2.65–4.17). 5 key findings →
Design: cross-sectional Participants: 2,798 Evidence: moderate
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117 participants have complete data (mean age: 73 ± 7.4). 5 key findings →
Design: cohort study Participants: 150 Evidence: moderate
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Fourteen articles met inclusion criteria after critical appraisal. 5 key findings →
Design: cross-sectional Evidence: high
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47/100
The method presented in this paper can be used to separate stable MCI patients from those who are at early stages of AD dementia with high accuracy. 2 key findings →
Participants: 86 Evidence: low
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Dysfunction of cholinergic basal forebrain (CBF) neurons of the nucleus basalis (NB) is a cardinal feature of Alzheimer's disease (AD) and correlates with cognitive decline. 3 key findings →
Evidence: low
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Degeneration of cholinergic nucleus basalis (NB) cortical projection neurons is associated with cognitive decline in late-stage Alzheimer's disease (AD). 3 key findings →
Evidence: low
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With tract-based spatial statistics and region-of-interest analyses, increased diffusivity in the extra-axonal space (extra-axonal axial and radial diffusivities) in several white matter tracts sensitively and accurately discriminated healthy controls from those with amnestic mild cognitive impairment (area under the receiver operating characteristic curve = 0.82-0.95), while widespread decreased axonal water fraction discriminated amnestic mild cognitive impairment from Alzheimer disease (area under the receiver operating characteristic curve = 0.84). 2 key findings →
Participants: 12 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 →