28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Biomarkers of the molecular pathology underpinning dementia syndromes are increasingly recognized as crucial for diagnosis and development of disease-modifying treatments. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tyrosine hydroxylase (TH), a rate-limiting step in catecholamine synthesis in which its activity influences Alzheimer disease, Parkinson disease, and IQ of schizophrenia patients, has been studied for a long time. 3 key findings →
Evidence: low
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Investigating new drugs or formulations that target Alzheimer disease (AD) is critical for advancing therapeutic interventions. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Expression of LRP1 by neurons in proximity to senile amyloid plaques does not appear to play a major role in modulating the formation of these proximal deposits or in the appearance of the associated neuritic pathology. 3 key findings →
Participants: 13 Evidence: low
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Clinical studies have shown that epileptic seizures worsen Alzheimer's disease (AD) pathology and related cognitive deficits; however, the underlying mechanism is unclear. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The apolipoprotein E genotype (APOE) is an established risk factor for Alzheimer disease, with the age-at-onset occurring earlier in individuals having at least one APOE epsilon 4 allele, relative to the APOE epsilon 3 or APOE epsilon 2 isoforms. 2 key findings →
Evidence: low
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Despite important inroads into the molecular pathology of Alzheimer disease, effective long-term treatment for the condition remains elusive. 3 key findings →
Evidence: low
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The frequency of the epsilon 4 allele of the apolipoprotein E (apoE) is increased in familial and sporadic late-onset Alzheimer's disease, but its prevalence in non-Alzheimer dementias in Caucasian populations is unknown. 1 key finding →
Evidence: low
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Alzheimer disease (AD) is a heterogeneous and progressive neurodegenerative disease, which in Western society mainly accounts for senile dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We completed a systematic survey of the human genome, conducted at an average resolution of 10 cM, for the identification of simple sequence tandem repeat polymorphisms (SSTRPs) that target new risk genes for Alzheimer disease (AD) by virtue of linkage disequilibrium. 5 key findings →
Evidence: low
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The objective of this study was to evaluate the effect of apolipoprotein E (APOE) epsilon 4 allele on regional cerebral perfusion (rCBF) changes using arterial spin labeling (ASL) magnetic resonance imaging (MRI) in subjects who are carriers or noncarriers of this risk factor for Alzheimer disease (AD). 5 key findings →
Evidence: low
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Despite the persistence of memory loss, the patients experienced a prompt and sustained response to mirtazapine. 2 key findings →
Evidence: high
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Clinical trial registration www. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There are many who feel that the achievement of a disease-modifying (DM) designation for a drug is an important goal in Alzheimer disease (AD) therapeutics. 5 key findings →
Evidence: high
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A person affected by Alzheimer's disease (AD) gradually loses the ability to perform activities of daily living and becomes dependent on caregivers, thereby having a negative impact on the caregivers' quality of life. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Epidemiological and experimental studies have suggested that high dietary intake of fats is associated with cognitive decline and a significantly increased risk of dementia. 4 key findings →
Evidence: low
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Imaging of brain β-amyloid plaques with (18)F-labeled tracers for PET will likely be available in clinical practice to assist the diagnosis of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The neurotrophin hypothesis proposes that repetitive neuronal activity enhances the expression, secretion and actions of neurotrophins to modify synaptic transmission and connectivity thereby providing a connection between neuronal activity and synaptic plasticity. 3 key findings →
Evidence: low
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The objective was to summarize recent findings about the clinical features, diagnosis and investigation of dementia with Lewy (DLB) bodies, together with its neuropathology, neurochemistry and genetics. 3 key findings →
Evidence: low
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Disability, characterised by the loss of ability to perform activities of daily living (ADL), is a defining feature of dementia that results in growing caregiver burden and the eventual need for alternative care or nursing home placement. 3 key findings →
Evidence: low
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Taiwan's accelerated rate of aging is more than twice that of European countries and United States. 5 key findings →
Evidence: low
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Among women, the number of years spent living with dementia for Whites, Blacks, U.S.-born Hispanics, and foreign-born Hispanics was 1.6, 3.9, 4.7, and 6.0 years, respectively. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is a well-documented tendency for cognitive tests to underestimate the abilities of older people in black and minority ethnic groups. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
It has remained a matter of debate until now whether amyloid and tangle pathology may be regarded as the main causes of the dementia in Alzheimer's disease (AD) or only as markers of the disease. 3 key findings →
Evidence: low
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This article reports findings from three linked qualitative research projects that explored how Australian general practitioners (GPs) spoke about their experiences in diagnosing dementia and their views on early diagnosis and barriers towards early diagnosis. 5 key findings →
Evidence: low
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 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.
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 →