Logopenic progressive aphasia (LPA) is a distinctive variant of primary progressive aphasia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
CSF tau and 18 F-AV-1451 have equal performance in early clinical stages of AD, but 18 F-AV-1451 is superior in the dementia stage, and exhibits close to perfect diagnostic performance for mild to moderate AD. 3 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings suggest that patterns of cortical Aβ and tau do not differ in people with PD-CN, people with PD-MCI, and healthy older adults. 5 key findings →
Design: cross-sectional Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Stroke is a leading cause of disability, dementia and death worldwide. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Across Latin American and Caribbean countries (LACs), the fight against dementia faces pressing challenges, such as heterogeneity, diversity, political instability, and socioeconomic disparities. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Attenuation of racial inequalities in older age can be extended to cognitive outcomes, which probably reflects selective survival. 1 key finding →
Design: cross-sectional Participants: 3,875 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In the present study, our automated classifier successfully classified FTD clinical subtypes with good to excellent accuracy. 1 key finding →
Participants: 143 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These results suggest that bvFTD may be characterized by an allostatic-interoceptive overload manifested in ongoing electrophysiological markers, brain atrophy, functional networks, and cognition. 4 key findings →
Participants: 94 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Traumatic brain injury (TBI), particularly of greater severity (i.e., moderate to severe), has been identified as a risk factor for all-cause dementia and Parkinson's disease, with risk for specific dementia subtypes being more variable. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
56/100
Alzheimer's disease and frontotemporal dementia (FTD) can be difficult to differentiate clinically because of overlapping symptoms. 5 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Metabolomics identified key disease-related metabolic changes and disease-progression-related changes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid-β oligomers may cause cognitive deficits in Alzheimer's disease by impairing neuronal NMDA-type glutamate receptors, whose function is regulated by the receptor tyrosine kinase EphB2. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a progressive neurodegenerative disease in which the formation of extracellular aggregates of amyloid beta (Aβ) peptide, fibrillary tangles of intraneuronal tau and microglial activation are major pathological hallmarks. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) pathology is defined by β-amyloid (Aβ) plaques and neurofibrillary tau, but Lewy bodies (LBs; 𝛼-synuclein aggregates) are a common co-pathology for which effective biomarkers are needed. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The CDR® plus NACC FTLD was able to detect early symptoms in the mildly impaired participants who were rated as CDR® sum of boxes (CDR®-SB) = 0. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Progressive cognitive decline in combination with a cerebrospinal fluid biomarker pattern of low levels of amyloid-β1-42 and high levels of total tau and phosphorylated tau is typical of Alzheimer's disease. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Among non-Latino Whites, ADI was associated with dementia incidence (most vs. least disadvantaged ADI quintile HR = 1.09, 95% confidence interval [CI] = 1.02-1.15). 4 key findings →
Participants: 18,103 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
56/100
After adjusting for demographics, apolipoprotein E (APOE) ε4 status, cognition, and comorbidities, the highest tertile of REM latency was associated with higher Aβ burden (β = 0.08, 95% confidence interval [CI]: 0.03 to 0.13, p = 0.002), elevated p-tau181 (β = 0.19, 95% CI: 0.02 to 0.13, p = 0.002), and reduced BDNF levels (β = -0.47, 95% CI: -0.68 to -0.13, p = 0.013), compared to the lowest tertile. 5 key findings →
Participants: 128 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Symptomatic females with genetic FTD had lower frontal cortical thickness than males, and the C9orf72 subgroup showed lower-than-expected frontal cortical thickness for a given level of executive functioning. 5 key findings →
Design: longitudinal study Participants: 394 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
56/100
ADNI participants (921 dyads) had a mean (SD) age of 71 (7) years and mean (SD) of 17 (3) years of education; 485 (53%) were female, 30 (3%) were Asian, 105 (11%) were Black, and 756 (82%) were White. eVAL participants (279 dyads) had a mean (SD) age of 71 (8) years and mean (SD) of 17 (2) years of education; 151 (54%) were female, 17 (6%) were Asian, 12 (4%) were Black, and 245 (88%) were White. 5 key findings →
Design: cross-sectional Participants: 921 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Nuclear depletion and cytoplasmic aggregation of the RNA-binding protein TDP-43 are cellular hallmarks of amyotrophic lateral sclerosis (ALS). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
55/100
Despite differences in prevalence of APOE-ε4, its association with dementia risk was similar across Chinese, Japanese, Filipino, and non-Latino White participants. 2 key findings →
Design: cohort Participants: 46,325 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Amyloid PET and sleep duration information was acquired on 4425 cognitively unimpaired participants (mean [SD] age, 71.3 [4.7] years; 2628 [59.4%] female; 1509 [34.1%] tested Aβ positive). 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Blood-based biomarkers offer a major advance in the clinical evaluation of neurodegenerative diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In addition, hippocampal sclerosis was a common neuropathological comorbidity ( n = 5) and associated with limbic-predominant TDP-43 proteinopathy ( n = 4) or FTLD-TDP ( n = 1). 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →