αSyn-PMCA is almost invariably positive in the CSF of patients with PAF establishing this condition as α-synucleinopathy. 1 key finding →
Participants: 32 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.
αSyn-PMCA is almost invariably positive in the CSF of patients with PAF establishing this condition as α-synucleinopathy. 1 key finding →
Participants: 32 Evidence: low
Full summary, score breakdown and related studies → Original source
The present data indicate that CSF NfL and t-tau levels reflect distinct pathophysiological mechanisms of neurodegeneration and support the clinical use of NfL as a fast screening biomarker for the differential diagnosis of atypical/rapidly progressive NDs. 4 key findings →
Participants: 141 Evidence: low
Full summary, score breakdown and related studies → Original source
Astrocytes play a formative role in memory consolidation during physiological conditions; when dysregulated, astrocytes release glial fibrillary acidic protein (GFAP), which has been linked with negative memory outcomes in animal studies. 3 key findings →
Participants: 69 Evidence: low
Full summary, score breakdown and related studies → Original source
Increased NFL levels are a common feature in neurodegenerative dementias. 2 key findings →
Participants: 122 Evidence: low
Full summary, score breakdown and related studies → Original source
Our results provide support for the continued study of plasma biomarkers as a clinical screening tool for AD and VCID pathology. 4 key findings →
Participants: 90 Evidence: low
Full summary, score breakdown and related studies → Original source
The MMSE score, MoCA score, serum miR-27a-3p level, cerebrospinal fluid miR-27a-3p, Aβ42 levels and Aβ42/Aβ40 ratio of AD patients in mild group and moderate-to-severe group were all lower than those in the control group, and the moderate-to-severe group were lower than the mild group (all P < 0.05);the serum NEAT1 level, SUVR, and cerebrospinal fluid NEAT1 and BACE1 levels were higher than those in the control group, and the moderate-to-severe group were higher than the mild group (all P < 0.05). 1 key finding →
Participants: 41 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma Aβ40, Aβ42, and P-Tau proteins in the NC, aMCI, and AD groups increased with the progression of AD ( P < 0.01); cortical thickness reductions in the AD-aMCI groups and AD-NC groups mainly involved the bilateral superior temporal gyrus, transverse temporal gyrus, superior marginal gyrus, insula, right entorhinal cortex, right fusiform gyrus, and cingulate gyrus. 1 key finding →
Participants: 33 Evidence: low
Full summary, score breakdown and related studies → Original source
CSF biomarkers may improve the accuracy of the modified Boston criteria with altered profile in 85% of the patients fulfilling revised Boston criteria for probable CAA. 3 key findings →
Participants: 63 Evidence: low
Full summary, score breakdown and related studies → Original source
Quantifying physical differences of protein aggregates implicated in Alzheimer’s disease (AD), in blood, could provide crucial information on disease stages. 1 key finding →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitive impairment and altered CSF biomarker concentrations indicative of AD pathology can predict increased mortality in patients with an AHF, and so probably even before clinical dementia diagnosis by early biomarker analysis; a notion that may have substantial clinical implications by improving perioperative treatment and postoperative rehabilitation. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Despite existing criteria, differential diagnosis of Vascular Dementia (VD) and Alzheimer's disease (AD) remains difficult. 3 key findings →
Participants: 92 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Most genetic studies concerning risk genes in Alzheimer's disease (AD) are from Caucasian populations, whereas the data remain limited in the Chinese population. 4 key findings →
Participants: 3,604 Evidence: low
Full summary, score breakdown and related studies → Original source
This study is the first to find protective associations of serum ApoB with CSF AD core biomarkers, especially in SCD individuals. 5 key findings →
Participants: 507 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma Aβ42 and Aβ40 are critically influenced by kidney function; however, their ratio is advantageously spared from this effect. 3 key findings →
Participants: 30 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Serum NFL levels were markedly elevated may be a useful clinical biomarker for discriminating PD patients from ET and controls. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Only Aβ burden measured by PET, but not markers of neuroinflammation, differed among cognitively unimpaired elderly with different APOE ε4 gene dose. 3 key findings →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source
We believe this is the first study to investigate associations between blood metabolites and neocortical amyloid burden (NAB) in the search for a blood-based biomarker for Alzheimer's disease (AD). 1 key finding →
Participants: 91 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Non-elevated plasma p-tau181 results impacted the diagnosis and use of amyloid PET imaging in a memory clinic. 5 key findings →
Design: cohort Participants: 100 Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
: Despite all scientific efforts and many protracted and expensive clinical trials, no new drug has been approved by FDA for treatment of Alzheimer disease (AD) since 2003. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
It has been well documented that neurotrophins, including brain-derived neurotrophic factor (BDNF), are severely affected in Alzheimer's disease (AD), but their administration faces a myriad of technical challenges. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
One hundred forty-six participants were examined (age 72 ± 6 years). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Several recent research studies show high performance of blood biomarkers to identify Alzheimer's disease also in the pre-dementia mild cognitive impairment (MCI) stage, but data from the routine clinical care memory clinic setting are needed. 1 key finding →
Participants: 54 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Treatment-resistant schizophrenia does not appear to be associated with neuronal, particularly axonal degeneration. 4 key findings →
Participants: 82 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The gFC was reduced in MC compared with NC participants. 5 key findings →
Design: cross-sectional Participants: 171 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Three-hundred seventy nine participants underwent blood draw (71.9 ± 7.8 years old, 60.2% female, 57% Hispanic of which 88% were Cuban or South American) and 240 completed Aβ-PET. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →