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
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
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
We examine a recent dispute regarding the Centers for Medicare and Medicaid Services' (CMS) refusal to unconditionally pay for amyloid positron emission tomography (PET) imaging for Medicare beneficiaries being assessed for Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accurate spatial normalization (SN) of amyloid positron emission tomography (PET) images for Alzheimer's disease assessment without coregistered anatomical magnetic resonance imaging (MRI) of the same individual is technically challenging. 1 key finding →
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
Non-linear relations of brain amyloid beta (Aβ) with task- based functional connectivity (tbFC) measured with functional magnetic resonance imaging (fMRI) have been reported in late middle age. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Alzheimer's disease (AD) is the most common cause of dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Posterior cortical atrophy (PCA), considered a visual variant of Alzheimer's disease, has similar pathological characteristics yet shows a selective visual manifestation with relative preservation of other cortical areas, at least at early stages of disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases target specific large-scale neuronal networks, leading to distinct behavioral and cognitive dysfunctions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aging is known to have deleterious effects on cerebral white matter, yet little is known about these white matter alterations in advanced age. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative brain changes can affect the functional connectivity strength between nodes of the default-mode network (DMN), which may underlie changes in cognitive performance. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Using AI for dementia diagnosis is still in research stage, however some of the work points to the development of new medical devices. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Locus of control (LOC) is an important personality trait. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The retina offers a unique "window" to study pathophysiological processes of dementia in the brain, as it is an extension of the central nervous system (CNS) and shares prominent similarities with the brain in terms of embryological origin, anatomical features and physiological properties. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The ensuing upward shift in demographic distribution due to the increase in life expectancy has resulted in a rising prevalence of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The AT(N) research framework was introduced in 2018 to define Alzheimer's disease as a biological entity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Differential diagnosis of atypical Parkinson syndromes (APS) is difficult as clinical presentations may vary and as there is a strong overlap between disease entities. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia is a syndrome characterised by chronic, multi-domain, acquired cognitive impairment that causes significant functional limitations. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is recognized as multifactorial and heterogeneous disease with multiple contributors to its pathophysiology, including vascular dysfunction. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with comparable degree of neuropathology could show different cognitive impairments. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 2,885 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.
- Exercise interventions preserve hippocampal volume: A meta-analysis
- PET imaging of amyloid deposition in patients with mild cognitive impairment
- Neonate hippocampal volumes: prematurity, perinatal predictors, and 2-year outcome
- Postmortem MRI and histology demonstrate differential iron accumulation and cortical myelin organization in early- and late-onset Alzheimer's disease
- Apolipoprotein E epsilon 4 allele and hippocampal volume in twins with normal cognition
- When, where, and how the corpus callosum changes in MCI and AD: a multimodal MRI study
- Identifying Genetic Risk for Amyloid-Related Imaging Abnormalities
- Mediterranean diet habits in older individuals: associations with cognitive functioning and brain volumes
- Imaging Vascular Disease and Amyloid in the Aging Brain: Implications for Treatment
- Alzheimer-related altered white matter microstructural integrity in Down syndrome: A model for sporadic AD?
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →