Postmortem MRI scans were obtained for the first 56 participants of the Nun Study who were scanned. 1 key finding →
Participants: 56 Evidence: low
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28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Postmortem MRI scans were obtained for the first 56 participants of the Nun Study who were scanned. 1 key finding →
Participants: 56 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Oxidative damage occurs in the brain of subjects with mild cognitive impairment, suggesting that oxidative damage may be one of the earliest events in the onset and progression of Alzheimer disease. 3 key findings →
Evidence: low
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Oxidative stress is thought to play a role in the pathogenesis of Alzheimer's disease (AD) and increased oxidative DNA damage has been observed in brain tissue from AD patients. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The histopathologic changes distinguishing early Alzheimer disease (AD) from normal or pathologic aging are not clearly defined. 5 key findings →
Participants: 29 Evidence: low
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Amyloid plaques and neurofibrillary tangles (NFTs) are the pathological hallmarks of Alzheimer disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Lipid peroxidation is one of the major outcomes of free radical-mediated injury that directly damages membranes and generates a number of secondary products, both from fission and endocyclization of oxygenated fatty acids that possess neurotoxic activity. 5 key findings →
Evidence: low
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Alzheimer disease (AD) is characterized neuropathologically by intracellular neurofibrillary tangles (NFT) and of extracellular senile plaques (SP), the central core of which is amyloid beta-peptide (Abeta) derived from amyloid precursor protein (APP), a transmembrane protein. 4 key findings →
Evidence: low
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Frontotemporal dementia with inclusion body myopathy and Paget disease of bone is a rare, autosomal-dominant disorder caused by mutations in the gene valosin-containing protein (VCP). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mild cognitive impairment (MCI) is generally referred to the transitional zone between normal cognitive function and early dementia or clinically probable Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Patients with MCI showed no significant difference (P>.05) in the number of diffuse plaques from that in normal controls or patients with EAD. 3 key findings →
Evidence: low
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Previous studies show increased levels of lipid peroxidation and neurotoxic by-products of lipid peroxidation including 4-hydroxynonenal (HNE) and acrolein in vulnerable regions of the Alzheimer's disease (AD) brain. 5 key findings →
Evidence: low
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Numerous investigations point to the importance of oxidative imbalance in mediating AD pathogenesis. 5 key findings →
Evidence: low
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A number of studies reported that oxidative and nitrosative damage may be important in the pathogenesis of Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The association of neurofibrillary tangles with delayed verbal recall may reflect associated hippocampal atrophy. 2 key findings →
Evidence: low
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Increasing evidence supports a role for oxidative damage in the pathogenesis of Alzheimer's disease (AD). 2 key findings →
Evidence: low
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Mild cognitive impairment (MCI), the earliest clinically detectable phase of the trajectory toward dementia and Alzheimer's disease (AD), led to the need for even earlier detection and prevention of AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Early Alzheimer's disease (EAD) is the intermediary stage between mild cognitive impairment (MCI) and late-stage Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Free radical-mediated oxidative damage is thought to play a role in the pathogenesis of Alzheimer disease. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive decline in multiple cognitive domains. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Two major risk factors for late-onset familial and sporadic Alzheimer disease (AD), a leading cause of dementia worldwide, are increasing age and inheritance of the epsilon4 allele of the apolipoprotein E gene (APOE4). 5 key findings →
Evidence: low
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All cells rely on efficient protein synthesis in order to maintain cellular homeostasis. 2 key findings →
Evidence: low
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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
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.
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 28,580 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →