30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer´s disease is considered a neurodegenerative disease and is diagnosed by exclusion, while the detection of specific cerebrospinal fluid (CSF) biomarkers, namely amyloid-beta (Aβ) peptides Aβ1-42 (Aß42), phospho-tau (181P; P-tau), and total-tau (T-tau), has been shown to improve diagnostic accuracy. 4 key findings →
Participants: 29 Evidence: low
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Autosomal dominant Alzheimer disease (ADAD) is caused by pathogenic variants in the APP, PSEN1 and PSEN2 genes, but a substantial fraction of reported variants is of unknown clinical significance. 4 key findings →
Evidence: low
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The NfL assay met analytical criteria, with precision demonstrating coefficients of variation <3% across runs, a lower limit of quantification of 3.10 pg/mL, linearity with <12% deviation, and <10% interference. 5 key findings →
Participants: 20 Evidence: low
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Roughly 32 million people worldwide live with Alzheimer disease, yet the vascular contributions to its progression remain incompletely mapped. 5 key findings →
Participants: 94 Evidence: moderate
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Hypertensive patients also had significantly lower thiol levels compared to those without hypertension (p < 0.05).Conclusion Our findings suggest that total and native thiol levels decline with cognitive deterioration and advancing age. 4 key findings →
Participants: 128 Evidence: low
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This position is justified by the fact that not all individuals with positive biomarkers will progress to symptomatic disease, as well as by the considerable variability in biomarker results depending on the type of marker and the laboratory performing the analysis (3).Both frameworks agree that biomarkers enhance diagnostic certainty but differ in the degree of reliance placed upon them. 5 key findings →
Evidence: low
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In 1906, Alois Alzheimer first described the neuropathological hallmarks of the disease that now bears his name. 2 key findings →
Participants: 62 Evidence: moderate
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Neurodegenerative dementias with behavioral clinical presentation are a diverse group of diseases. 4 key findings →
Participants: 20 Evidence: moderate
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DNA methylation, mRNA and protein levels, and cognitive performance using the Mini-Mental State Examination (MMSE) and Clock Drawing Test (CDT). 3 key findings →
Evidence: low
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Alzheimer's disease (AD) and frontotemporal dementia can often be diagnosed accurately with careful clinical history, cognitive testing, neurological examination, and structural brain MRI. 1 key finding →
Evidence: low
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Detection of cerebrospinal fluid (CSF) biomarker deviations improve prediction of progression from mild cognitive impairment (MCI) to dementia. 4 key findings →
Participants: 161 Evidence: low
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This review addresses recent developments in the analyses of plasma amyloid beta (Aβ) and total tau (t-tau) protein levels as biomarkers for discriminating amnestic mild cognitive impairment (aMCI) from Alzheimer disease (AD), using immunomagnetic reduction (IMR). 4 key findings →
Evidence: low
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The goals of this study were to compare the early diagnostic utility of Alzheimer disease biomarkers in the CSF with those in brain MRI in conditions found in our clinical practice, and to ascertain the diagnostic accuracy of both techniques used together. 4 key findings →
Participants: 30 Evidence: low
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Autoantibody-associated psychiatric syndromes are a novel disease entity that is not fully understood. 4 key findings →
Evidence: moderate
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Technical developments have paved the way for the development of ultrasensitive analytical methods that allow for precise quantification of brain-specific proteins in blood samples. 4 key findings →
Evidence: low
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The 2018 NIA-AA research framework proposes a classification system with beta- A myloid deposition, pathologic T au, and n eurodegeneration (ATN) for the diagnosis and staging of Alzheimer’s Disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The development of more effective disease-modifying treatments for Alzheimer's disease (AD) is compromised by the lack of streamlined measures to detect and monitor the full spectrum of neurodegeneration, including white matter pathology, which begins early. 2 key findings →
Evidence: low
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Evaluate the performance of emerging Alzheimer disease (AD) plasma biomarkers in a specialty memory clinic. 1 key finding →
Evidence: low
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Eight proteins were differently expressed in carriers with larger WMH volumes (Figure 1). 5 key findings →
Evidence: low
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LCN2 is not only a potential biomarker for the early diagnosis of AD but may also play a significant role in the neurodegenerative processes associated with the disease. 5 key findings →
Evidence: low
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CSF pTau181/Ab42 ratio is a diagnostic marker for Alzheimer disease correlated well with PET scan compared to various standalone cognitive screening assessment. 5 key findings →
Participants: 40 Evidence: low
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The full length TDP-43 assay in standard format had a quantitative range of 10-275,000 pg/mL and sufficient sensitivity to quantitate 100% of the tested plasma samples. 5 key findings →
Evidence: low
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The nervous system specific proteins glial fibrillary acidic protein (GFAp), S-100 and myelin basic protein (MBP) were determined in 535 human cerebrospinal fluid (CSF) samples. 2 key findings →
Evidence: low
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There is a need for improvement of the diagnosis of vascular dementia (VaD). 5 key findings →
Evidence: low
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Cortical posterior hypometabolism on PET imaging with 18 F-FDG (FDG-PET), and altered levels of Aß 1-42 peptide, total Tau (tTau) and phosphorylated Tau (pTau) proteins in cerebrospinal fluid (CSF) are established diagnostic biomarkers in Alzheimer's disease (AD). 4 key findings →
Participants: 120 Evidence: low
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10 of the 939 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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