Oxidative stress is deeply involved in multiple pathological processes of VaD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Oxidative stress is deeply involved in multiple pathological processes of VaD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vascular dementia (VaD) is a neurodegenerative disorder characterized by chronic oxygen insufficiency, leading to the generation of oxygen-free radicals, inflammatory responses, disturbances in iron metabolism, lipid peroxidation, and other pathological changes that disrupt intracellular homeostasis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this review, we outline the significant roles of necroptosis and its molecular mechanisms in the pathological process of VaD, with a particular focus on the role of necroptosis in modulating neuroinflammation and exacerbating the disruption of BBB permeability in VaD, and elaborate on the molecular regulatory mechanisms and the centrally involved cells of necroptosis mediated by tumor necrosis factor-α in neuroinflammation in VaD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Gait disturbances (odds ratio (OR) = 19.32; p = 0.01), visual-spatial complaints (OR = 6.06; p = 0.03), and visual hallucinations (OR = 31.06; p = 0.002) predicted DLB compared to AD, along with better memory (OR = 3.42; p = 0.003), naming (OR = 3.35; p = 0.002), and worse processing speed (OR = 0.51; p = 0.01). 5 key findings →
Evidence: low
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The spectral analysis of the resting-state eyes-closed electroencephalographic (rsEEG) activity typically shows abnormal delta (< 4 Hz), theta (4-7 Hz), and alpha (8-12 Hz) power in older patients with cognitive deficits due to progressive neurodegenerative diseases. 4 key findings →
Evidence: low
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: Integrating clinical bioinformatics with computational drug design, this study establishes a translational paradigm for nanomaterial development. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We observed adults aged 50 years and older from the UK Biobank over a median observational period exceeding two years following COVID-19 infection. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tau aggregation driven by microtubule-associated protein tau (MAPT) mutations is central to frontotemporal dementia pathology, yet no disease-modifying therapies effectively target mutant tau. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
• To clarify the key role of Muscone delayed the development of vascular dementia (VD). • To reveal synaptic function in VD associated with neuronal pentraxin receptor (NP2). • To reveal that Muscone alleviates VD through the BDNF-TrkB-NP2 signaling pathway initially. 3 key findings →
Evidence: low
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Parkinson's disease is the second most common neurodegenerative disease, after Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aggregation of alpha-synuclein, an abundant and conserved pre-synaptic brain protein, is implicated as a critical factor in several neurodegenerative diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found a significantly greater intensity of cytoplasmic immunostaining for HDAC4 and HDAC6 in granule cells of the dentate gyrus in cases of FTLD overall compared with controls, and specifically in cases of FTLD tau‐ P icks compared with FTLD tau‐ MAPT and controls. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Three Newcastle patients bearing an expansion in C9ORF72 were identified. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
How does the brain maintain to-be-remembered information in working memory (WM), particularly when the focus of attention is drawn to processing other information? 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The enzyme pair PINK1 and PRKN together orchestrates a cytoprotective mitophagy pathway that selectively tags damaged mitochondria with phospho-serine 65 ubiquitin (pS65-Ub) and directs them for autophagic-lysosomal degradation (mitophagy). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Graph theory has proven to be useful in studying brain dysfunction in Alzheimer’s disease using MagnetoEncephaloGraphy (MEG) and fMRI signals. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This is the first reported case of AIWS in a patient with DLB. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal lobar degeneration (FTLD) represents a heterogeneous group of neurodegenerative disorders with overlapping clinical, pathological, and genetic characteristics. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The results showed that bilinguals had reduced thalamic volume compared to monolinguals despite having similar cognitive performance. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vascular dementia (VaD) is recognized as the second most prevalent form of dementia after Alzheimer's disease, with its pathogenesis intricately associated with cerebrovascular pathologies, including chronic hypoperfusion, oxidative stress, and neuroinflammation. 2 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Familial frontotemporal dementia (FTD) is a genetically heterogeneous disease with various clinical manifestations, making it difficult to diagnose. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frequently occurring copathology, most commonly with Alzheimer disease, leads to greater cognitive decline, increased likelihood of admission to a long-term care facility, and a higher risk of mortality. 1 key finding →
Evidence: low
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Dementia with Lewy bodies (DLB) and Parkinson's Disease (PD) are common causes of motor and cognitive deficits and are associated with the abnormal accumulation of alpha-synuclein (α-syn). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study supports the notion that defects in the autophagy pathway and more specifically in mTor and Atg7 are associated with neurodegeneration in DLB cases and alpha-synuclein transgenic models and supports the possibility that modulators of the autophagy pathway might have potential therapeutic effects. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
ResultsThe CNR2 missense variant rs4649124 was associated with increased vascular dementia risk (BH-adjusted P = 0.049) after correction at the 5% false discovery rate (FDR) threshold, with additional associations at the 10% FDR threshold for all-cause dementia risk (BH-adjusted P = 0.051) and lower circulating APP (BH-adjusted P = 0.088) and BDNF (BH-adjusted P = 0.083) levels. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 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.
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 →