28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by neuronal loss, extracellular amyloid-β (Aβ) plaques, and intracellular neurofibrillary tau tangles. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The early diagnosis of neurodegenerative disorders is still an open issue despite the many efforts to address this problem. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is one of the most common causes of dementia worldwide. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is a pressing need for novel diagnostic and progression biomarkers of neurodegeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau protein is a key target of interest in developing therapeutics for neurodegenerative diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An accurate diagnosis of sporadic cerebral amyloid angiopathy (CAA) is critical for patient management and research (including clinical trials) for this common small vessel pathology of the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Small vessel disease (SVD) is one of the most frequent pathological conditions which lead to dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrovascular pathologies occur in up to 80% of cases of Alzheimer's disease; however, the underlying mechanisms that lead to perivascular pathology and accompanying blood-brain barrier (BBB) disruption are still not fully understood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alterations in cerebral blood flow are common in several neurological diseases among the elderly including stroke, cerebral small vessel disease, vascular dementia, and Alzheimer's disease. 4D flow magnetic resonance imaging (MRI) is a relatively new technique to investigate cerebrovascular disease, and makes it possible to obtain time-resolved blood flow measurements of the entire cerebral arterial venous vasculature and can be used to derive a repertoire of hemodynamic biomarkers indicative of cerebrovascular health. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Limbic-predominant age-related TDP-43 encephalopathy (LATE) is a recently defined neurodegenerative disease characterized by amnestic phenotype and pathological inclusions of TAR DNA-binding protein 43 (TDP-43). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
α-syn aggregates represent the pathological hallmark of synucleinopathies as well as a frequent copathology (almost 1/3 of cases) in AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The CSF level of Ng was significantly higher, whereas the NPTXR was significantly lower in the AD patients than in cognitively healthy controls. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A diverse set of biological processes have been implicated in the pathophysiology of Alzheimer's disease (AD) and related dementias. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hispanic family caregivers of people with dementia experience higher levels of stress compared to non-Hispanic white caregivers. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Differentially methylated positions (DMPs) between persons with and without late-onset Alzheimer's disease (LOAD) were observed at 477 of 769,190 loci in a plurality of genes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In BriefIn the search for biomarkers of synapse loss associated with Alzheimer's disease (AD), we used shotgun proteomics to identify a panel of 9 synaptic proteins detectable in human cerebrospinal fluid (CSF).Expression at the human synapse was verified using super resolution microscopy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
To study the potential diagnostic value of abnormally phosphorylated tau protein in Creutzfeldt-Jakob disease (CJD) compared to Alzheimer's disease (AD), we determined levels of tau phosphorylated at threonine 231 (p-tau231) and of total tau (t-tau) in cerebrospinal fluid (CSF) of CJD patients, AD patients, and healthy controls (HC). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Assay drift may reduce statistical power or even confound analyses. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuropsychological tests, CSF markers, and hippocampal volume predicted conversion from MCI to AD and general dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Familial Alzheimer's disease (AD) due to PSEN1 mutations provides an opportunity to examine AD biomarkers in persons in whom the diagnosis is certain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent studies show that fibrinogen plays a role in the pathogenesis of Alzheimer's disease (AD), which may be crucial to neurovascular damage and cognitive impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Overall, these results support the vervet as a non-human primate model of amyloid-related neurodegeneration, such as Alzheimer's disease and cerebral amyloid angiopathy, and highlight Aβ 1-40 and p-tau 181 as potentially valuable biomarkers of these processes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the diagnosis of Alzheimer's disease (AD) total tau (T-tau), tau phosphorylated at threonine 181 (P-tau181), and the 42 amino acid isoform of alpha β-amyloid (Aβ) are well established surrogate CSF markers. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Between 1992 and 2000, 8 women developed dementia (4 AD, 3 vascular dementia, 1 mixed vascular dementia and AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although the use of cerebrospinal fluid (CSF) amyloid β1-42 (Aβ42), tau (T-tau), and phosphorylated tau (p-tau181) gives added diagnostic and prognostic values, the diffusion is still limited in clinical practice and only a restricted number of patients receive an integrated clinico-biological diagnosis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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.
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 →