In 1906, Alois Alzheimer first described the neuropathological hallmarks of the disease that now bears his name. 2 key findings →
Participants: 62 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neurodegenerative dementias with behavioral clinical presentation are a diverse group of diseases. 4 key findings →
Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
Aceruloplasminemia is an interesting disease, the study of which helps elucidate how iron-induced oxidative stress is involved in neuronal cell death. 2 key findings →
Evidence: low
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We investigated a possible role in Alzheimer's disease (AD) for FKBP12, a peptidyl-prolyl cis-trans isomerase known to be important in protein assembly, folding and transportation by using Western blotting and microscopic analyses in postmortem brain tissues from elderly controls and the patients with AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
34/100
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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S100beta is a soluble protein released by glial cells mainly under the activation of the 5-HT1A receptor. 2 key findings →
Evidence: low
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Cerebrospinal fluid (CSF) total Tau levels vary widely in neurodegenerative disorders, thus being not useful in their discrimination over Alzheimer disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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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The objective of this study was to investigate the levels of tau protein in neurosyphilis. 4 key findings →
Participants: 12 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
Full summary, score breakdown and related studies → Original source Free full text
The BACE1 gene encodes the beta-site APP-cleaving enzyme 1 and has been associated with Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Autoantibody-associated psychiatric syndromes are a novel disease entity that is not fully understood. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
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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Transgenic mice expressing the oncogenic protein-serine/threonine kinase Mos at high levels in the brain display progressive neuronal degeneration and gliosis. 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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From across this tag
10 of the 3,322 studies in this tag, 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.
- Alpha-synuclein co-pathology in Down syndrome-associated Alzheimer's disease
- Dementia etiology classification using NULISA plasma biomarkers and machine learning
- Behavioral phenotyping of GFAP-apoE3 and -apoE4 transgenic mice: apoE4 mice show profound working memory impairments in the absence of Alzheimer's-like neuropathology
- Alzheimer Disease, Vascular Disease, and Blood-Brain Barrier Permeability Biomarkers in Middle-Aged Adults
- Brain derived β-interferon is a potential player in Alzheimer's disease pathogenesis and cognitive impairment
- Genetic architecture of Alzheimer’s disease-related plasma biomarkers
- Plasma p-tau217 detects Alzheimer's disease co-pathology in cerebral amyloid angiopathy: Comparison to CSF biomarkers in the ANGMAR cohort
- Plasma phosphorylated tau 217 concentrations, APOE genotype, and timing of cognitive impairment in individuals across diverse racial and ethnic groups: a pooled analysis of prospective cohort studies
- Vocal acoustic biomarkers predict amyloid positivity in non-demented individuals
- Resveratrol Attenuates CSF Markers of Neurodegeneration and Neuroinflammation in Individuals with Alzheimer's Disease
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →