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
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
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 development of blood-based biomarkers of Alzheimer's disease (AD) pathology as tools for screening the general population, and as the first step in a multistep process to determine which non-demented individuals are at greatest risk of developing AD dementia, is essential. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The effects of applying clinical versus neuropathological diagnosis and the inclusion of cases with coincident neuropathological diagnoses have not been assessed specifically when studying cerebrospinal fluid (CSF) biomarker classification cutoffs for patients with neurodegenerative diseases that cause dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Further studies will refine this model and enable the use of biomarkers studied in ADNI clinically and in disease-modifying therapeutic trials. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
(a) the novel Aβ1-40 and Aβ1-42 ELISA assays characterize with very good analytical performance; (b) we reconfirm that the CSF Aβ42/40 concentration ratio shows significantly better diagnostic performance compared to the CSF Aβ1-42 concentration alone. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This review provides a concise overview of recent advances in cerebrospinal fluid (CSF) and blood-based biomarkers of Alzheimer's disease lesions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Combining the biomarker panel allows differentiating between various types of neurodegenerative dementias and contributes to a better understanding of their pathophysiological processes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
It is not well known whether Alzheimer's disease (AD) cerebrospinal fluid (CSF) biomarkers are associated with brain damage in cognitively normal elderly. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia affecting 60%-70% of people afflicted with this disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid and tau biomarkers for Alzheimer's disease are widely recognized diagnostic tools for the identification of Alzheimer's disease pathology antemortem and are recommended by the most recent clinical and research guidelines. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Treatment of Alzheimer's disease (AD) is significantly hampered by the lack of easily accessible biomarkers that can detect disease presence and predict disease risk reliably. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the public health crisis of the 21st century. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent findings Plasma biomarkers have significantly improved our understanding of ADRD time-course, risk factors, diagnosis and prognosis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-biomarker-based tests are highly important for the early clinical diagnosis of Alzheimer's disease (AD) and the treatment and care of AD patients, but the complex serum environment and extremely low abundance of AD blood protein biomarkers present challenges. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Substances produced throughout the body are detectable in the blood, which is the most common biological fluid used in clinical testing. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disease that causes cognitive impairments in areas such as memory, language, and reasoning. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disease and the single commonest cause of dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
An unmet need exists for reliable plasma biomarkers of amyloid pathology, in the clinical laboratory setting, to streamline diagnosis of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this clinical study the cerebrospinal fluid (CSF) level of a novel form of the beta-amyloid peptide (A beta) extending to position 42 (A beta 42) was determined in patients with Alzheimer's disease (AD) as well as controls. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease, as a most prevalent type of dementia, is quickly becoming one of the most expensive, lethal, and burdening diseases of this century. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) pathology is estimated to develop many years before detectable cognitive decline. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau immunoreactivity was studied in temporal neocortex, area 22, in 15 cases with graded intellectual status and compared with the immunoreactivity observed with an antiserum against paired helical filaments (PHF) and with the density of amyloid revealed by thioflavin S. Samples came from women over 75 years either intellectually normal or affected by senile dementia of the Alzheimer type at various degrees of severity. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The elevated level of cerebrospinal fluid (CSF) Tau and phosphorylated Tau181 (p-Tau181) proteins are well established hallmarks of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The number of patients with Alzheimer's Disease (AD) and other types of dementia disorders has drastically increased over the last decades. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Previous studies on blood-based biomarkers for Alzheimer's disease suggest a less invasive blood test might be a valuable screening tool for Alzheimer-specific pathology. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 707 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 →