The E693Delta mutation has been suggested as a cause of dementia because of enhanced formation of synaptotoxic Abeta oligomers. 2 key findings →
Participants: 2,121 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Amyloid deposition is associated with lower cognitive performance both in AD patients and in the normal elderly, but the association is modified by CR, suggesting that CR may be protective against amyloid-related cognitive impairment. 4 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
The PET Core has demonstrated a variety of methods for the standardization of biomarkers such as florbetapir PET in a multicenter setting. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
We have investigated the extent and pattern of immunostaining for ubiquitin protein (UBQ) in 60 patients with frontotemporal lobar degeneration (FTLD) with ubiquitin-positive, tau-negative inclusions (FTLD-U), 37 of whom were ascertained in Manchester UK and 23 in Newcastle-Upon-Tyne, UK. 1 key finding →
Participants: 60 Evidence: low
Full summary, score breakdown and related studies → Original source
Idiopathic rapid eye movement sleep behaviour disorder is characterized by nocturnal violence, increased muscle tone during rapid eye movement sleep and the lack of any other neurological disease. 2 key findings →
Participants: 21 Evidence: low
Full summary, score breakdown and related studies → Original source
These results indicate that RNFL and RNFL+GCL thickness measurements are reduced in AD patients compared with healthy subjects. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The contributors to persistent cognitive impairment and hippocampal atrophy in leucine-rich glioma-inactivated 1 antibody encephalitis (LGI1) patients are unknown. 2 key findings →
Participants: 124 Evidence: low
Full summary, score breakdown and related studies → Original source
All six CTE stage III cases had Braak NFT stage III but no neuritic plaques. 5 key findings →
Design: clinical trial Participants: 39 Evidence: low
Full summary, score breakdown and related studies → Original source
[18F]PI-2620 is a second generation tracer that has shown high binding affinity for tau aggregation in Alzheimer's disease (AD). 2 key findings →
Participants: 49 Evidence: low
Full summary, score breakdown and related studies → Original source
The aAD patients showed significantly higher tau accumulation, relative hypoperfusion and grey matter density loss in the temporal lobes compared to PCA and lvPPA patients. 5 key findings →
Participants: 32 Evidence: low
Full summary, score breakdown and related studies → Original source
We investigated self-rating of cognitive task performance (self-appraisal) and the difference between self-rating and actual task performance (appraisal discrepancy) in cognitively healthy older adults and their relationship with cortical thickness and Alzheimer's disease (AD) biomarkers, amyloid and tau. 4 key findings →
Participants: 151 Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with 4R-tauopathies in contrast to non-4R-tauopathies were detected at higher sensitivity in the 20-40-minute frame (common: 79%, scaled: 76%) compared to the 40-60-minute frame (common: 55%, scaled: 62%), albeit with reduced specificity in the common setting (20-40-min: 78%, 40-60-min: 95%), which was ameliorated in the intensity-scaled setting (20-40-min: 91%, 40-60-min: 96%). 5 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
We compared regional retention of 18F-flortaucipir between 20 patients with Lewy body disorders (LBD), 12 Alzheimer's disease patients with positive amyloid positron emission tomography (PET) scans (AD+Aβ) and 15 healthy controls with negative amyloid PET scans (HC-Aβ). 1 key finding →
Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source
SUVR using the whole cerebellum as the reference region and centiloid (CL) cutoffs for early and established amyloid pathology were 1.10 (13.5 CL) and 1.24 (35.7 CL), respectively. 5 key findings →
Participants: 287 Evidence: low
Full summary, score breakdown and related studies → Original source
Four of the 17 patients (23.5%) had amyloid-β pathology based on the overall pathology read and also showed increased [(18)F]flutemetamol uptake. [(18)F]Flutemetamol standardized uptake values from the biopsy site were significantly associated with biopsy specimen amyloid-β levels (Pearson's r = 0.67; p = 0.006). 5 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
Aβ1-42, tTau and pTau (but not Aβ1-40) and the ratios with Aβ1-42 had good diagnostic agreement with 18 F-Florbetapir PET. 4 key findings →
Participants: 35 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyloid-PET presented higher diagnostic accuracy, sensitivity, and NPV than CSF Aβ1-42 but not Aβ42/40 ratio. 5 key findings →
Participants: 148 Evidence: low
Full summary, score breakdown and related studies → Original source
In the negative images of the HS group, the contrast between the white matter and the gray matter was high in the FMM PET images, while striatal uptake was relatively higher in the FPN PET images. 5 key findings →
Participants: 605 Evidence: low
Full summary, score breakdown and related studies → Original source
50/100
Twenty-five/38 (65.8%) amyloid PET/CT scans resulted positive for amyloid deposition. 5 key findings →
Participants: 38 Evidence: low
Full summary, score breakdown and related studies → Original source
We assessed the severity of amyloid-β accumulation and white matter lesions (WML) in the brain, and their association with cognitive decline, in patients (n = 47) with Alzheimer's disease (AD). 4 key findings →
Participants: 47 Evidence: low
Full summary, score breakdown and related studies → Original source
The neuropathology of Parkinson's disease dementia (PDD) is heterogenous, and the impacts of each pathophysiology and their synergistic effects are not fully understood. 2 key findings →
Participants: 23 Evidence: low
Full summary, score breakdown and related studies → Original source
Multimodal biomarkers may identify former contact sports athletes with repeated concussions and at risk for dementia. 3 key findings →
Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD), affecting nearly 6.5 million people, is the fifth leading cause of death in individuals 65 years or older in the USA. 4 key findings →
Participants: 32 Evidence: low
Full summary, score breakdown and related studies → Original source
50/100
As of 2023, it is estimated that 6.7 million individuals in the United States live with Alzheimer's disease (AD). 3 key findings →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source
50/100
WMH volume within the inferior fronto-occipital fasciculus (IFOF) was the highest among all tract ROIs and associated with reduced FC in IFOF-connected DMN areas, independently of global AV-45 PET. 3 key findings →
Participants: 78 Evidence: low
Full summary, score breakdown and related studies → Original source
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →