Alzheimer's disease (AD) is a devastating form of dementia, with the number of affected individuals rising sharply. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) is a devastating form of dementia, with the number of affected individuals rising sharply. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Higher socioeconomic status and increased frequency of physical activity were associated with a lower risk of both EOD and LOD. 5 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The number of people living with dementia is expected to rise to 153 million cases globally by 2050. 4 key findings →
Participants: 17,500 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Lewy body dementia (LBD) encompasses neurodegenerative dementias characterized by cognitive fluctuations, visual hallucinations, and parkinsonism. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) represent two extremes of a neurodegenerative disease spectrum characterised by overlapping genetic, clinical, and neuropathological features. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal dementia is a debilitating neurodegenerative disorder characterized by frontal and temporal lobe degeneration, resulting in behavioral changes, language difficulties, and cognitive decline. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
AD patients exhibited a significant reduction in the water exchange rates across the BBB, whereas DLB patients showed a significant increase in BBB permeability to contrast agent. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Compared to controls, PSP and bvFTD had lower values of midbrain area, HBS-RS and GMA, and higher MRPI and MRPI 2.0. 3 key findings →
Participants: 19 Evidence: low
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Nonsense mutations generate premature termination codons (PTCs) that are responsible for 11% of genetic disease alleles. 2 key findings →
Evidence: low
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Patients with DLB with anxiety had a significantly higher percentage of fluctuating cognition than those without anxiety. 4 key findings →
Participants: 40 Evidence: low
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Microstructural alterations in brain tissue play a crucial role in the pathophysiology of frontotemporal dementia (FTD). 1 key finding →
Evidence: low
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We observed a nonlinear trajectory of two functional connectivity metrics-temporal variability (fluidity) and connectedness (average node strength)-across symptom severity, especially in the delta frequency band. 4 key findings →
Participants: 39 Evidence: low
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Of 44,899 MCI patients, 6391 progressed to AD. 5 key findings →
Evidence: low
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Gender has an impact on CR, but not through socio‐economic variables. 2 key findings →
Participants: 440 Evidence: moderate
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Forty-four physicians, primarily neurologists (n = 31; 70.5 %), were interviewed. 5 key findings →
Participants: 31 Evidence: low
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Making early and informative diagnoses of mild cognitive impairment (MCI) is highly important for planning timely and appropriate interventions aimed at dementia risk reduction. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Fifty-nine patients fulfilled the inclusion criteria. 5 key findings →
Design: case-control study Evidence: moderate
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A total of 90 (38.96%) participants were healthy and 141 (61.04%) had MCI. 5 key findings →
Design: cross-sectional Participants: 231 Evidence: low
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Whereas neurotoxic Aβ is derived from amyloid precursor protein (APP) by β- and γ-secretase cleavage, APP processing along the non-amyloidogenic pathway results in the secretion of the large neurotrophic ectodomain APPsα. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Although the relationship between macroautophagy/autophagy and Alzheimer disease (AD) is widely studied, the underlying mechanisms are poorly understood, especially the regulatory role of the initiation signaling of autophagy on AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Familial Alzheimer's disease (FAD) is caused by dominant missense mutations in amyloid precursor protein (APP) and presenilin-1 (PSEN1), the catalytic component of γ-secretase that generates amyloid β-peptides (Aβ) from the APP C-terminal fragment C99. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Of 138 (27%) eligible patients (46% female, age 61 ± 8 years, Mini-Mental State Examination [MMSE] 22 ± 6), 75 (54%) underwent genetic testing. 5 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Individual cognitive profiles of patients with Parkinson's disease dementia (PDD) are highly heterogeneous, suggesting possible biological subtypes. 1 key finding →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The efficacy of acetylcholinesterase inhibitors (AChEI) and memantine (ME) in severe dementia remains uncertain, and real world data are limited. 4 key findings →
Participants: 703 Evidence: moderate
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Multivariable linear regression analysis indicated that being married (β = 0.6, p-value = 0.02) and being a young adult (β = 0.52, p-value = 0.04) were significantly associated with better neurocognitive performance. 1 key finding →
Design: cross-sectional Participants: 59 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.
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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events