27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
A great number of epidemiological studies have demonstrated that the frequency of the epsilon4 allele of the apolipoprotein E gene (APOE) is markedly higher in sporadic and in familial late onset Alzheimer disease (AD). 3 key findings →
Evidence: low
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The aims of this study were to identify risk factors for hip fracture in men aged 50 years or more. 5 key findings →
Evidence: low
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Parkinson's disease (PD) is a neurodegenerative disorder that is pathologically characterized by the presence of intracytoplasmic Lewy bodies, the major components of which are filaments consisting of alpha-synuclein. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The appearance of inflammatory markers associated with amyloid plaques indicates a state of chronic inflammation in Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Microglia are a major ghal component of the central nervous system (CNS) and are extremely sessile. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is the most common cause of dementia in the elderly, and the fourth leading cause of death in the United States. 4 key findings →
Evidence: low
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Recently intronic and exonic mutations in the Tau gene have been found to be associated with familial neurodegenerative syndromes characterized not only by a predominantly frontotemporal dementia but also by the presence of neurological signs consistent with the dysfunction of multiple subcortical neuronal circuitries. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
GMHR is a reliable, valid, global bedside measure of severity of general medical comorbidity for patients with dementia that can be used for clinical and research purposes. 1 key finding →
Participants: 819 Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic exposure to increased glucocorticoid concentrations appears to lower the threshold for hippocampal neuronal degeneration in the old rat. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
Mutations in the beta-amyloid precursor protein are strongly associated with some cases of familial Alzheimer's disease. 3 key findings →
Design: cross-sectional Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
Letter and category fluency tasks are used to assess semantic knowledge, retrieval ability, and executive functioning. 1 key finding →
Participants: 365 Evidence: low
Full summary, score breakdown and related studies → Original source
The epsilon 4 allele of apolipoprotein E (APOE) has been found to be a risk factor for late-onset Alzheimer's disease (AD). 1 key finding →
Evidence: low
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Attention to three themes may help clinicians and investigators meet the challenge of treating the common mental disorders of later life: the effect of these disorders on functioning, prevention of the consequences of mental disorders, and integration of mental health care and primary health care services. 2 key findings →
Evidence: low
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There is overwhelming evidence to suggest that the neuropathology of Alzheimer disease (AD) extends beyond amyloid plaques and neurofibrillary tangles. 2 key findings →
Evidence: low
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Amyloid precursor protein (APP) plays a central role in Alzheimer disease. 4 key findings →
Evidence: low
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Lack of insight or impaired awareness of deficits in patients with dementia is a relatively neglected area of study. 4 key findings →
Participants: 37 Evidence: low
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Microglia are the main human immunodeficiency virus (HIV) reservoir in the central nervous system and most likely play a major role in the development of HIV dementia (HIVD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There have, however, been few studies which have sought to investigate factors associated with carer burden and differences and similarities between countries. 5 key findings →
Evidence: low
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Despite these good results in the CAPIT scores, one patient experienced a partially regressive corticobulbar syndrome with dysphagia, dysarthria, and increased drooling. 4 key findings →
Evidence: low
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Down syndrome is caused by over-expression of genes located within a segment of chromosome 21, termed the Down locus. 2 key findings →
Evidence: low
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The present investigation examined the validity of the revised Hopkins Verbal Learning Test (HVLT-R). 3 key findings →
Evidence: low
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Senile plaques composed of A beta peptides are a histopathological hallmark of Alzheimer disease (AD). 4 key findings →
Evidence: low
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We surveyed the medical records of outpatients meeting the NINCDS-ADRDA criteria for probable DAT who were able to complete the Cognitive Difficulties Scale (CDS) and had a close informant relative (IR) who could complete the family form of the same questionnaire. 4 key findings →
Participants: 88 Evidence: low
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The preclinical stage of Alzheimer's disease is inconspicuous and there are - almost by definition - no reliable and valid symptoms and signs which would allow a very early diagnosis before the manifestation of irreversible deficits. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease (AD) is the commonest form of adult onset dementia and is characterised neuropathologically by the accumulation of plaques containing beta-amyloid (A beta) fibrils, reactive astrocytes, activated microglia, and leukocytes. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →