27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
These findings suggest that APOE genotype has a differential effect on the distribution of amyloid plaques and glucose metabolism. 2 key findings →
Evidence: low
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Apolipoprotein (apo) E, a multifunctional protein with central roles in lipid metabolism and neurobiology, has three common isoforms (apoE2, apoE3, and apoE4) with different effects on lipid homeostasis and neurobiology. 2 key findings →
Evidence: low
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The association of neurofibrillary tangles with delayed verbal recall may reflect associated hippocampal atrophy. 2 key findings →
Evidence: low
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Several recent autopsy studies suggest that senile dementia of Lewy body type (SDLT) may be the second most common neuropathologic cause of dementia in the elderly, accounting for 7 to 30% of all cases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Apraxia of speech, NVOA, and ideomotor apraxia are at least partially separable disorders. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Review of clinical and biological features of primary progressive aphasia (PPA). 2 key findings →
Evidence: low
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This well-characterized case of PCA syndrome due to AD in a very young patient with DS demonstrates the occurrence of atypical presentations in DS that might be overshadowed by the baseline intellectual disability associated with DS. 5 key findings →
Evidence: low
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This article discusses why CSF biomarkers found in normal-pressure hydrocephalus (NPH) can be misleading when distinguishing NPH from comorbid NPH with Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In vivo [ 18 F]-AV-1451 PET neuroimaging was performed in 5 patients with sporadic CJD (median age, 66 years [63-74]), and results were compared to cognitively normal (CN) persons (n = 44; median age, 68 years [63-74]) and to participants with very mild Alzheimer disease (AD) dementia (n = 8; median age, 77 years [63-90]). 4 key findings →
Participants: 44 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) and frontotemporal lobar degeneration (FTLD) may have overlapping clinical presentations despite distinct underlying neuropathologies, thus making in vivo diagnosis challenging. 4 key findings →
Participants: 185 Evidence: low
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Eighty patients were included (mean age: 81 years, interquartile range 74-86 years; 36.2% female, ∼80% with dementia and Alzheimer disease). 5 key findings →
Evidence: low
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= 0.039) were associated with better global cognition. 5 key findings →
Evidence: low
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< 0.1). -ε4 status, and Aβ load, and not mediated by markers of neuroaxonal degradation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A 59-year-old man developed problems with reading and driving. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Thirty cases of diffuse Lewy body disease (DLBD) have been reported, primarily by neuropathologists, but an associated clinical syndrome has not been clearly defined. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Drug development for Alzheimer disease and other neurodegenerative dementias, including frontotemporal dementia, has experienced a long history of phase 2 and phase 3 clinical trials that failed to show efficacy of investigational drugs. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical trials to advance the diagnosis and treatment of Alzheimer disease (AD) may expose research subjects to discrimination risks. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Despite the presumptive common underlying neuropathology of amyloid plaques and neurofibrillary tangles, the 2 groups displayed 2 different patterns of network perturbation, each concordant with the clinical presentation and the anatomy of neurodegeneration. 2 key findings →
Participants: 14 Evidence: low
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The results of this study suggest that dyslipidemia increases the risk of plaque-type pathology. 3 key findings →
Evidence: low
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Because NAA is considered a marker of neuronal integrity, reduced medial temporal and parietal lobe NAA could be an early indication of dementia-related pathology in elderly individuals. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
= 0.032). In individuals with LOUE, elevated plasma p-tau217 was associated with both cognitive impairment and disrupted sleep microarchitecture, with the most pronounced cognitive deficits observed in individuals with medication refractory epilepsy. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
= 0.036), with lower scores in PCA and lvPPA (median 21 and 21, respectively) compared with CBS-AD (median 27). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Blood-based biomarkers (BBMs) for Alzheimer disease (AD) offer widely expanded access to biomarker-informed diagnoses in community settings that have previously lacked such resources. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Glial fibrillary acidic protein (GFAP), a protein that is associated with 9-nm filaments of astrocytes, was observed to be increased in the astrocytes surrounding senile plaques in patients with Alzheimer dementia and in aged subjects without dementia. 2 key findings →
Evidence: low
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In chronic liver failure, manganese accumulation is responsible for the pallidal MRI T1 hyperintensity. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
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.
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.
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 →