Commercial advertising of computerized "brain games" may result in clinicians being asked whether brain games prevent dementia. 4 key findings →
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.
The apolipoprotein E (apoE) gene has been implicated in various conditions, most notably Alzheimer's disease and coronary artery disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In a cell free assay, ADAM10 activity was found to be significantly lower in apoE4 samples compared to apoE2. 7WCHO cells over expressing wild type AβPP exposed to apoE4 demonstrated reduced formation of sAβPPα compared to other apoE isoforms. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulation and aggregation of amyloid-β (Aβ) in the brain is an initiating step in the pathogenesis of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We aimed to summarize the recent advances in genetic findings of Alzheimer's disease (AD), focusing on traditional single-marker and gene approaches and non-traditional ones, i.e., polygenic and epistatic components. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is heritable with complex genetic underpinnings. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia play an important role in mediating inflammatory processes in the central nervous system (CNS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia, which has been currently considered as a genetically complex disorder caused by a combination of environmental and genetic risk factors. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
The Dominantly Inherited Alzheimer's Network (DIAN) observational study compared pathophysiological markers between mutation carriers and non-carriers in autosomal dominant Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
MicroRNAs are small non-coding RNAs that function as regulators of gene expression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in PSEN1 are responsible for familial Alzheimer's disease (FAD) inherited as autosomal dominant trait, but also de novo mutations have been rarely reported in sporadic early-onset dementia cases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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
Nine PD patients (35%) were identified with mild cognitive impairment. 5 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
Alzheimer's disease (AD) is a chronic neurodegenerative disorder and the most common cause of dementia among the elderly population. 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
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
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
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
Dementia with Lewy bodies (DLB) is a common form of dementia and is characterized by cognitive fluctuations, visual hallucinations, and Parkinsonism. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
In bilateral parietotemporal areas, oscillatory envelope amplitude increased with healthy ageing, whereas both local amplitude and node-to-global connectivity decreased with AD. 5 key findings →
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 →