27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
As part of a cross-national study of dementia epidemiology, two types of verbal fluency tasks were administered to three groups of subjects, varying in level of literacy and education, recruited from the rural district of Ballabgarh in northern India. 2 key findings →
Evidence: low
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Neurofibrillary tangles (NFTs) form in a number of neurodegenerative disorders. 2 key findings →
Evidence: low
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Frontotemporal dementia (FTD) is a dementia syndrome characterized by peculiar behavioral changes arising from frontotemporal involvement and distinct from Alzheimer's disease (AD). 4 key findings →
Design: post-hoc analysis Evidence: low
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We conducted a single-stage community-based study of dementia on all registered residents > or =65 years in age in a rural Chinese community. 2 key findings →
Evidence: low
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Twenty formal carers employed in three nursing homes narrated 92 episodes of lucidity (ELs) in people with severe dementia. 5 key findings →
Evidence: low
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The presenilin-1 (PS1) gene mutation (Pro117Leu), recently identified in a Polish family is characterized by the earliest reported onset (from 24-31 years) of Alzheimer disease (AD) and a very short duration of disease (4-6 years). 3 key findings →
Evidence: low
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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
Frontotemporal dementia is a neurological disorder characterised by personality changes, deterioration of memory and executive functions as well as stereotypical behaviour. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The hypothesis is forwarded that sporadic late-onset Alzheimer disease is caused by non-insulin dependent diabetes mellitus which is confined to the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A group of similar autosomal dominant hereditary neurodegenerative disorders have been linked to chromosome 17 in thirteen kindreds. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Renal failure is relatively common, but except in association with spina bifida or paraplegia it is unlikely to occur as a result of disease of the CNS. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The present study examined the relationship between visual attention measures and driving performance in healthy older adults and individuals with very mild and mild dementia of the Alzheimer type (DAT). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Theories of the pathophysiology of schizophrenia have implicated the hippocampus, but controversy remains regarding hippocampal abnormalities in patients with schizophrenia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Delayed memory impairments and medial temporal-lobe atrophy are considered to be cardinal features of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our results provide some support for the lateralised model of material specific memory deficits, but suggest that a number of demographic and epilepsy-related factors may interact with the extent and laterality of hippocampal pathology in shaping the nature of the associated neuropsychological deficit. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Nitric oxide (NO) is a unique biological messenger molecule which mediates diverse physiologic roles. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cytokines and chemokines have been implicated in contributing to the initiation, propagation and regulation of immune and inflammatory responses. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Inflammatory processes may play a critical role in the pathogenesis of the degenerative changes and cognitive impairments associated with Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The epsilon4 allele of apolipoprotein E (apoE) is associated with increased risk for Alzheimer's disease (AD) and poor outcome after brain injury. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Excessive cerebral accumulation of the 42-residue amyloid beta-protein (Abeta) is an early and invariant step in the pathogenesis of Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Activated monocytes release a number of substances, including inflammatory cytokines and eicosanoids, that are highly toxic to cells of the central nervous system. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E, alpha2-macroglobulin, and amyloid precursor protein (APP) are involved in the development of Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
It is a truism of modern biomedical science that the development of therapies expected to slow or arrest the progression of a disease requires as detailed an understanding of its molecular and cellular pathogenesis as possible. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
EEG coherence can be used to evaluate the functionality of cortical connections and to get information about the synchronization of the regional cortical activity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
According to the amyloid hypothesis for the pathogenesis of Alzheimer's disease (AD), amyloid beta peptide (Abeta) directly affects neurons, leading to neurodegeneration and tau phosphorylation, followed by the production of paired helical filaments (PHF) in neurofibrillary tangles (NFT). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 →