30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Cerebral small vessel disease (CSVD) is a major yet underappreciated driver of cognitive impairment and dementia, contributing to nearly half of all cases. 1 key finding →
Evidence: low
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Serum IGF-1 concentration was significantly reduced in patients and rats with arteriosclerotic cSVD. 5 key findings →
Participants: 26 Evidence: low
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The associations of lower foveal capillary density with cerebral WMH and amyloid positivity suggest that further research is warranted to evaluate for shared mechanisms of disease between small vessel disease and AD pathologies. 5 key findings →
Participants: 41 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Quantification of in vivo amyloid and tau PET imaging relationships with postmortem measurements are critical for validating the sensitivity and specificity imaging biomarkers across clinical phenotypes with Alzheimer disease neuropathologic change (ADNC). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vitamin D and vitamin D receptor (VDR) have been postulated as environmental and genetic factors in neurodegeneration disorders including multiple sclerosis (MS), Alzheimer disease (AD), and recently Parkinson disease (PD). 5 key findings →
Evidence: moderate
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Cognitive impairment (CI) is a common nonmotor complication of Parkinson's disease (PD), and is associated with significant disability for patients and burden for caregivers. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A well-documented feature of Huntington's disease (HD) is disproportionate impairment in the ability to recognise the emotional expression of disgust. 2 key findings →
Evidence: low
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Parkinson's disease patients may suffer from cognitive impairment and behavioural problems such as apathy, personality changes, speech disturbances and visual hallucinations (Parkinson's disease dementia). 5 key findings →
Evidence: low
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Patients with degenerative dementia often show language disorders, but little is known about their verbal (VC) and non-verbal communication (NVC). 2 key findings →
Evidence: low
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Patients with advanced Parkinson's disease had a significantly higher disease impairment, longer disease duration, and an unstable motor response to levodopa with frequent on-off fluctuations. 5 key findings →
Participants: 29 Evidence: low
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The profile of aphasia suggests that primary progressive aphasia tends to affect anterior parts of the language-dominant cortex first. 5 key findings →
Evidence: low
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An 82-year-old man presented with progressive changes in personality, social conduct, and executive function with preservation of memory, deteriorating from baseline to requiring acute hospitalization within 6 months. 1 key finding →
Design: case report Evidence: low
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The proteinopathy sporadic Parkinson's disease (sPD) is the second most frequent degenerative disorder of the human nervous system after Alzheimer's disease. 1 key finding →
Evidence: low
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Recent studies have shown that neurofibrillary tangles are frequently accompanied by alpha-synuclein inclusions in sporadic and familial Alzheimer disease, in Down syndrome, in progressive supranuclear palsy, and Parkinsonism dementia complex of Guam. 2 key findings →
Evidence: low
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For these neurodegenerative dementias, we observed that the chronological age did not align with their biological age, which was determined based on hippocampal transcript levels (i.e., transcriptional age). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
White matter hyperintensities (WMH) on MRI scans indicate lesions of the subcortical fiber system. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Both DLB and DAT groups exhibited impaired performance across the range of tasks designed to assess semantic memory. 4 key findings →
Evidence: low
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In 4 cases of Parkinson's disease (PD), 2 cases of Dementia with Lewy bodies (DLB) and 3 age-matched controls, the TUNEL/ISEL method was used to detect DNA fragmentation in substantia nigra locus coeruleus and cerebral cortex [method by Gold et al. In addition, immunohistochemistry was performed for an array of apoptosis-related proteins, i.e. the recently described apoptosis specific protein cJun/AP1 (ASP), the proto-oncogenes c-Jun, c-Jun AP1, Bcl2, Bax, Bcl-x, p53, CD 95 (Fas/Apo-1) 4 key findings →
Evidence: low
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HEK293, Neuro2a and SH-SY5Y expressing increased levels of α-synuclein were treated with sonicated α-synuclein pre-formed fibrils, to model seeded aggregation. 1 key finding →
Evidence: low
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IRMA can be used to learn and disregard center-specific information in features extracted from brain $$^{18}$$ 18 F-FDG PET scans, while retaining disease-specific information. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia is a growing problem of global relevance, currently affecting over 55 million people worldwide. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Metabolomics provide a promising tool for understanding dementia pathogenesis and identifying novel biomarkers. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Accurate identification of neurodegenerative disorders, including Alzheimer’s Disease (AD) and Frontotemporal Dementia (FTD), is crucial for prompt medical intervention. 1 key finding →
Evidence: low
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There are increasing calls for sharing individual biomarker results with participants in dementia research. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The STUB1/CHIP holds promise as a potential biomarker for distinguishing between SCI subjects, AD, and FTD. 5 key findings →
Participants: 90 Evidence: low
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10 of the 2,748 studies in this tag that have a study page, 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.
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 30,180 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →