28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Traumatic brain injury (TBI) has been linked to the development of neurodegenerative diseases, particularly Alzheimer's disease (AD) and chronic traumatic encephalopathy (CTE). 2 key findings →
Evidence: low
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Transactive response DNA-binding protein of 43 kDa (TDP-43) and tau proteins play critical roles in neurodegenerative diseases, particularly frontotemporal lobar degeneration (FTLD) and Alzheimer's disease (AD). 2 key findings →
Evidence: low
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Sex influences cognitive aging and dementia, yet research on the impact of female-specific factors, such as parity and fetal sex, on later-life cognition remains limited and equivocal. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyotrophic lateral sclerosis (ALS) and Huntington disease (HD) are lethal neurodegenerative diseases affecting motor function. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Family caregivers had information, psychosocial, and self-care needs that were deeply intertwined and frequently coexisted at the same time. 5 key findings →
Evidence: low
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EOD participants reported the highest mean levels of all psychosocial outcomes (e.g., everyday discrimination score of 8.3 in EOD vs 4.6 in LOD and 6.8 in no-dementia). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is the most common form of dementia with hallmarks of β-amyloid deposits, neurofilament tangles, synaptic loss and neuronal death in the patient's brain. 5 key findings →
Evidence: low
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Stroke is a leading cause of death and disability globally, with significant long-term impacts such as post-stroke cognitive impairment (PSCI). 1 key finding →
Evidence: low
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Growing evidence highlights sex-related differences in the pathogenesis of Alzheimer's disease (AD). 1 key finding →
Evidence: low
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Compared to controls, MAO-B immunoreactive area fraction was significantly increased in the frontal cortex and white matter of AD, CBD, and especially PiD and FTLD-TDP, but not PSP. 5 key findings →
Participants: 20 Evidence: low
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While cerebrovascular dysfunction and reactive astrocytosis are extensively characterized hallmarks of Alzheimer's disease (AD) and related dementias, the dynamic relationship between reactive astrocytes and cerebral vessels remains poorly understood. 3 key findings →
Evidence: low
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One hundred and eighteen years have passed since Alzheimer's disease (AD) was first diagnosed by Alois Alzheimer as a multifactorial and complex neurodegenerative disorder with psychiatric components. 5 key findings →
Evidence: low
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Alzheimer's disease (AD) is one of the leading causes of dementia in the elderly, and no effective treatment is currently available. 4 key findings →
Evidence: low
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In AD-like mice surgery induced acute changes in amyloid-β; perioperative treatment with pVNS effectively reduced amyloid-β load, plaque sphericity, and neuronal loss. 5 key findings →
Evidence: low
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The accumulation of pathological four-repeat (4R) tau is central to several frontotemporal dementia (FTD) subtypes, but human neuronal models amenable to high-throughput screening of 4R tau-targeting therapies remain very limited. 1 key finding →
Evidence: low
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Tauopathies are neurodegenerative diseases characterized by the pathological accumulation of microtubule-associated protein tau (MAPT) in the brain. 3 key findings →
Evidence: low
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Repulsive guidance molecule-a (RGMa) has emerged as a significant therapeutic target in a variety of neurological disorders, including neurodegenerative diseases and acute conditions. 1 key finding →
Evidence: low
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Alzheimer's disease (AD), the most prevalent form of dementia, leads to progressive cognitive decline due to pathological hallmarks including amyloid plaques, neurofibrillary tangles, synaptic loss, neuroinflammation, and neuronal cell death, highlighting the urgent need for multitarget therapeutic strategies. 2 key findings →
Participants: 31 Evidence: low
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TMEM106B is a lysosome/late endosome protein that is a potent genetic modifier of multiple neurodegenerative diseases as well as general aging. 1 key finding →
Evidence: low
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This study aimed to examine the effects of aerobic and strength training methodologies, either combined with or without cognitive training, on mitigating cognitive decline. 5 key findings →
Participants: 56 Evidence: low
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The growing prevalence of dementia emphasizes the need for effective prevention strategies. 4 key findings →
Participants: 289 Evidence: low
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The manuscript provides a thorough analysis of the neurovascular and metabolic processes that contribute to cognitive deterioration in patients with Type 2 diabetes (T2D). 5 key findings →
Design: longitudinal study Evidence: moderate
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For the interim analysis as of October 2024, the results of the MCI study arm are reported (n=42). 5 key findings →
Participants: 42 Evidence: high
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Each 10% increase in UPF intake was associated with lower attention scores (-0.05 points) and higher dementia risk (+0.24 points), independent of Mediterranean diet adherence. 2 key findings →
Design: cross-sectional Evidence: low
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Dementia affects over 55 million people globally, with early cognitive decline, such as Mild Cognitive Impairment (MCI), often preceding neurodegenerative diseases. 1 key finding →
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 →