27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
In the first of five phases in the evolution of beta-amyloidosis Abeta deposits are found exclusively in the neocortex. 5 key findings →
Design: clinical trial Evidence: low
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In this study, levels of total A(beta)x-40 and A(beta)x-42 were elevated early in dementia and levels of both peptides were strongly correlated with cognitive decline. 4 key findings →
Design: cross-sectional Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source
Epidemiologic studies have reported that cancer survivors have a relatively low risk of developing dementia, but the mechanisms underlying that inverse relationship are mostly unknown. 4 key findings →
Participants: 8,121 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The TMEM106B risk variant was significantly enriched in AD cases with transactive response DNA-binding protein 43 kDa (TDP-43) pathology - associating with increased odds of developing AD TDP-43 subtype α - but failed to associate with Lewy body or vascular pathology. 3 key findings →
Participants: 2,604 Evidence: low
Full summary, score breakdown and related studies → Original source
Genomic triplication of the alpha-synuclein gene (SNCA) has been reported to cause hereditary early-onset parkinsonism with dementia. 4 key findings →
Evidence: low
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We report duplication of the APP locus on chromosome 21 in five families with autosomal dominant early-onset Alzheimer disease (ADEOAD) and cerebral amyloid angiopathy (CAA). 3 key findings →
Evidence: low
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The lesions of Alzheimer disease include accumulation of proteins, losses of neurons and synapses, and alterations related to reactive processes. 4 key findings →
Evidence: low
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Several families with an early-onset form of familial Alzheimer's disease have been found to harbour mutations at a specific codon (717) of the gene for the beta-amyloid precursor protein (APP) on chromosome 21. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Innate immunity is associated with Alzheimer's disease 1 , but the influence of immune activation on the production of amyloid-β is unknown 2,3 . 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Astrocytes fulfill neuronal trophic roles normally, but are transformed in Alzheimer disease (AD) into A1-type reactive astrocytes that may destroy neurons through unknown mechanisms. 2 key findings →
Participants: 28 Evidence: low
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Neuronal inclusions of poly(GA), a protein unconventionally translated from G4C2 repeat expansions in C9ORF72, are abundant in patients with frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) caused by this mutation. 4 key findings →
Evidence: low
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There is a growing literature on the importance of hippocampal volume in geriatric depression. 4 key findings →
Design: longitudinal study Participants: 66 Evidence: moderate
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We tested the hypothesis that BBB breakdown is associated with cognitive decline and inflammation in nondemented elders. 4 key findings →
Participants: 120 Evidence: low
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Co-pathologies play an important role in the expression of the Alzheimer's disease clinical phenotype and may influence treatment efficacy. 4 key findings →
Participants: 96 Evidence: low
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Braak stages of tau neurofibrillary tangle accumulation have been incorporated in the criteria for the neuropathological diagnosis of Alzheimer's disease. 4 key findings →
Participants: 301 Evidence: low
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The critical role of primary care clinicians (PCCs) in Alzheimer's disease (AD) prevention, diagnosis and management must evolve as new treatment paradigms and disease-modifying therapies (DMTs) emerge. 4 key findings →
Evidence: low
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Study objective To describe a population that was categorized as "cognitively impaired not demented" (CIND) and to examine the utility of some of the proposed criteria for describing this degree of cognitive impairment. 4 key findings →
Design: longitudinal study Participants: 2,914 Evidence: moderate
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Loss of motor function is a common consequence of aging, but little is known about the factors that predict idiopathic motor decline. 4 key findings →
Design: cohort study Participants: 906 Evidence: moderate
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Researchers examined brains obtained at autopsy from nondemented and demented individuals to study extracellular amyloid deposits and intraneuronal neurofibrillary changes. 3 key findings →
Evidence: low
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Imaging and postmortem studies suggest that frontal lobe white matter (FLWM) volume expands until about the age of 44.6 years and then declines. 4 key findings →
Design: cross-sectional Participants: 34 Evidence: low
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Neurodegenerative diseases are characterised by neuronal loss and cerebral deposition of proteins with altered physicochemical properties. 4 key findings →
Participants: 233 Evidence: low
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Relating clinical symptoms to neuroanatomical profiles of brain damage and ultimately to tissue pathology is a key challenge in the field of neurodegenerative disease and particularly relevant to the heterogeneous disorders that comprise the frontotemporal lobar degeneration spectrum. 4 key findings →
Evidence: moderate
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We recently surveyed the relationship between the human brain transcriptome and genome in a series of neuropathologically normal postmortem samples. 4 key findings →
Participants: 188 Evidence: moderate
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No treatment for frontotemporal dementia (FTD), the second most common type of early-onset dementia, is available, but therapeutics are being investigated to target the 2 main proteins associated with FTD pathological subtypes: TDP-43 (FTLD-TDP) and tau (FTLD-tau). 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Magnetic resonance (MR) imaging is used widely for assessment of patients with cognitive impairment, but the pathological correlates are unclear, especially when multiple pathologies are present. 4 key findings →
Participants: 93 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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 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.
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 →