Diabetes mellitus is one of the major risk factors for cognitive dysfunction. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Diabetes mellitus is one of the major risk factors for cognitive dysfunction. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), a primary cause of dementia in the aging population, is characterized by extracellular amyloid-beta peptides aggregation, intracellular deposits of hyperphosphorylated tau, neurodegeneration and glial activation in the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most common form of dementia affecting elderly people. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The neurosensory retina emerges as a prominent site of Alzheimer's disease (AD) pathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We found a general trend of increased degree of asymmetry with increasing severity of diagnosis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neurodegenerative diseases, including Alzheimer, Parkinson, Huntington, and amyotrophic lateral sclerosis, are a prominent class of neurological diseases currently without a cure. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Machine learning models consistently outperformed conventional approach. 5 key findings →
Participants: 38,746 Evidence: low
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Frontotemporal dementia (FTD) is a neurodegenerative disorder primarily affecting the frontal and temporal lobes, leading to significant impairments in executive function, social behavior, and emotional regulation. 3 key findings →
Design: cohort study Evidence: moderate
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Amyloid-beta (Aβ) 42/40 ratio, tau phosphorylated at threonine-181 (p-tau), and total-tau (t-tau) are considered core biomarkers for the diagnosis of Alzheimer's disease (AD). 5 key findings →
Evidence: low
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Brain aging is central to late-onset Alzheimer's disease (LOAD), although the mechanisms by which it occurs at protein or cellular levels are not fully understood. 4 key findings →
Evidence: low
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Neurodegenerative diseases are characterized by protein aggregation and overlapping pathologies, challenging traditional classifications and highlighting shared underlying mechanisms. 1 key finding →
Evidence: low
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Alzheimer's disease (AD) affects over 6 million people over the age of 65. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mild cognitive impairment (MCI) is the prodromal stage of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical assessment of brain function relies heavily on indirect behavior-based tests. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Improved prediction of progression to Alzheimer's Disease (AD) among older individuals with mild cognitive impairment (MCI) is of high clinical and societal importance. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Obesity is a multifactorial disease in which environmental conditions and several genes play an important role in the development of this disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is a complex neurodegenerative disorder with no definite treatment. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyotrophic lateral sclerosis (ALS) is a fatal adult-onset neurodegenerative disorder affecting motor neurons (MNs). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mildly demented LBD patients had a significant deficit judging narratives compared to non-demented patients, but this deficit was not correlated with MMSE. 4 key findings →
Participants: 30 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
< 0.001) for both measures. When distinguishing NC from MCI/DM, the CIST outperformed the K-MMSE, demonstrating a higher AUC (0.869 vs. 0.842) and F1-score (0.697 vs. 0.409). 3 key findings →
Participants: 100 Evidence: low
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The human tau protein is implicated in a wide range of neurodegenerative "tauopathy" diseases, consisting of Alzheimer's disease (AD) and frontotemporal lobar degeneration which includes progressive supranuclear palsy, corticobasal degeneration, Pick's disease, and FTLD-tau (frontotemporal dementia with parkinsonism caused by MAPT mutations). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Biomarkers of neurodegeneration and neuronal injury have the potential to improve diagnostic accuracy, disease monitoring, prognosis, and measure treatment efficacy. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia are the resident macrophages of the central nervous system (CNS) acting as the first line of defense in the brain by phagocytosing harmful pathogens and cellular debris. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Currently, there is no disease-modifying treatment available for Alzheimer's and Parkinson's disease (AD and PD) and that includes the highly controversial approval of the Aβ-targeting antibody aducanumab for the treatment of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative condition characterized by tau pathology and accumulations of neurofibrillary tangles (NFTs) along with amyloid-beta (Aβ). 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 →