All seven patients showed elevated FTP uptake in the anterior temporal lobe with a leftward asymmetry that was not observed in healthy controls. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
B/AA individuals had elevated CP and HC SUVR (p < 0.007), whereas other ROI SUVR and HC SUVR covaried for CP SUVR did not show race differences (p > 0.05). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Highest agreement with [18F]FDG-PET quantification was reached for [18F]PI-2620-PET acquisition from 0.5 to 2.5 min p.i. for global mean (lowest R = 0.69) and cerebellar scaling (lowest R = 0.63). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
The subgroups showed the expected 18F-flortaucipir-binding patterns. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Retention of 18F-Flortaucipir is reportedly increased in the semantic variant of primary progressive aphasia (svPPA), which is dominated by TDP-43 pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Regional standardized uptake value ratios (SUVRs) for tau positron emission tomography (PET) were compared among 19 cognitively normal human immunodeficiency virus (HIV)-negative control individuals, 20 HIV-negative patients with symptomatic Alzheimer disease, 15 cognitively normal HIV-positive individuals, and 17 cognitively impaired HIV-positive individuals. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings suggested that occipitoparietal cortex, posterior cingulate cortex and precuneus, which were particularly affected by increased tau accumulation in VS-AD patients, may associate with visuospatial dysfunction of AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulation of paired helical filament tau contributes to neurodegeneration in Alzheimer's disease (AD). 18 F-flortaucipir is a positron emission tomography (PET) radioligand sensitive to tau in AD, but its clinical utility will depend in part on its ability to predict cognitive symptoms in diverse dementia phenotypes associated with selective, regional uptake. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
This study aimed to determine the pattern of [18F]flortaucipir uptake in individuals affected by Gerstmann-Sträussler-Scheinker disease (GSS) associated with the PRNP F198S mutation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disorder associated with extracellular plaques, composed of amyloid-beta (Aβ), in the brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Following the conversion of FBB or FMM SUVRs into CL units, a direct relationship was formed between the FBB or FMM SUVRs and the CL units using dcCL method (FBB dcCL = 151.42 × FBB dcSUVR - 142.24 and FMM dcCL = 148.52 × FMM dcSUVR - 137.09). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Reference region selection is important for proper amyloid PET analysis, especially in subcortical vascular dementia (SVaD) patients. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
18F-Florbetaben uptake was clearly visualized in the carotid arteries. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative condition characterized by progressive cognitive decline and memory loss, and is the most common form of dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Among the six cerebral cortical regions, the cingulate cortices and frontal lobe showed the highest SUVRs. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulation of amyloid beta can be visualized using [18F]florbetapir positron emission tomography. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Two patients were diagnosed with AD based on positive Amyloid PET imaging and were subsequently started on cholinesterase inhibitor treatment. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid positron emission tomography (PET) imaging enables in vivo detection of brain Aβ deposition, one of the neuropathological hallmarks of Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Amyloid plaques are a neuropathologic hallmark of Alzheimer's disease (AD), which can be imaged through positron emission tomography (PET) technology using radiopharmaceuticals that selectively bind to the fibrillar aggregates of amyloid-β plaques (Amy-PET). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early- and late-phase image fusion displayed with appropriate color tables is presented in three different cases to illustrate the added value of the suggested approach. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Loneliness is a perception of social and emotional isolation that increases in prevalence among older adults during the eighth decade of life. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The uptake of 18 F‐PI‐2620 was distinctly increased in the AD group across all the ROIs. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Both (18)F-FDG and (11)C-PiB imaging appear to be of limited use for predicting the progression from MCI to dementia due to AD in short-term follow-up, irrespective of the strategy of analysis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
38/100
Imaging of brain β-amyloid plaques with (18)F-labeled tracers for PET will likely be available in clinical practice to assist the diagnosis of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
We present a comparative split-half resampling analysis of various data driven feature selection and classification methods for the whole brain voxel-based classification analysis of anatomical magnetic resonance images. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
From across this tag
10 of the 1,160 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.
- Disturbed fluctuations of resting state EEG synchronization in Alzheimer's disease
- Neuronal loss correlates with but exceeds neurofibrillary tangles in Alzheimer's disease
- Hippocampal atrophy based Alzheimer's disease diagnosis via machine learning methods
- Comparison of three plasma p-tau217 assays to detect PET-confirmed Alzheimer's pathologies
- Diagnostic impact of [18F]flutemetamol PET in early-onset dementia
- Dual-Phase 18F-Florbetaben PET/CT: Unsuspected Thalamic Infarction Mimicking Alzheimer Disease
- The Vascular Hypothesis of Alzheimer's Disease: A Key to Preclinical Prediction of Dementia Using Neuroimaging
- Multisite study of the relationships between antemortem [ 11 C]PIB‐PET Centiloid values and postmortem measures of Alzheimer's disease neuropathology
- Patterns of tau pathology identified with 18 F-MK-6240 PET imaging
- Convolutional Neural Network Achieves 97.67 Percent Accuracy for Alzheimer MRI Classification
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 →