Dominant mutations in two DNA/RNA binding proteins, TDP-43 and FUS/TLS, are causes of inherited Amyotrophic Lateral Sclerosis (ALS). 4 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.
Dominant mutations in two DNA/RNA binding proteins, TDP-43 and FUS/TLS, are causes of inherited Amyotrophic Lateral Sclerosis (ALS). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Little is known about the relative benefits of cognitively stimulating activities at different points in the lifespan. 4 key findings →
Evidence: moderate
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Since the initial reports of coronavirus disease 2019 (COVID-19) in China in late 2019, infections from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have spread rapidly, resulting in a global pandemic that has caused millions of deaths. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vascular dementia (VaD) is widely recognised as the second most common type of dementia. 4 key findings →
Evidence: low
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We investigated the global placental gene expression profile in severe preeclampsia. 4 key findings →
Participants: 50 Evidence: low
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Inclusion body myopathy associated with Paget's disease of bone and frontotemporal dementia (IBMPFD) is a dominantly inherited degenerative disorder caused by mutations in the valosin-containing protein (VCP7) gene. 4 key findings →
Evidence: low
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The interstitial fluid (ISF) drainage pathway has been hypothesized to underlie the clearance of solutes and metabolites from the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The introduction of immunotherapy and its ultimate success will require re-evaluation of the pathogenesis of Alzheimer's disease particularly with regard to the role of the ageing microvasculature and the effects of APOE genotype. 4 key findings →
Evidence: low
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Despite a growing interest in auditory verbal hallucinations (AVHs) in different clinical and nonclinical groups, the phenomenological characteristics of such experiences have not yet been reviewed and contrasted, limiting our understanding of these phenomena on multiple empirical, theoretical, and clinical levels. 4 key findings →
Evidence: low
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Neuroimaging with iron-sensitive MR sequences [gradient echo T2* and susceptibility-weighted imaging (SWI)] identifies small signal voids that are suspected brain microbleeds. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The prevalence of a number of clinical features occurring in patients with early- (before age 65) and late-onset primary degenerative dementia of the Alzheimer type (PDDAT) are compared. 3 key findings →
Participants: 65 Evidence: low
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Alzheimer's disease (AD) is the most prevalent form of late-onset dementia. 4 key findings →
Evidence: low
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Autosomal dominant cerebellar ataxia, deafness and narcolepsy (ADCA-DN) is characterized by late onset (30-40 years old) cerebellar ataxia, sensory neuronal deafness, narcolepsy-cataplexy and dementia. 4 key findings →
Evidence: low
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Alzheimer disease (AD), a progressive neurodegenerative disorder, is the most common cause of dementia in the elderly. 4 key findings →
Evidence: low
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Neurodegeneration is a phenomenon that occurs in the central nervous system through the hallmarks associating the loss of neuronal structure and function. 4 key findings →
Evidence: low
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Alzheimer disease (AD) is a frequent and devastating neurodegenerative disease in humans, but still no curative treatment has been developed. 4 key findings →
Evidence: low
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Microglial activation is a key feature in Alzheimer's disease and is considered to contribute to progressive neuronal injury by release of neurotoxic products. 4 key findings →
Evidence: low
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The importance of (micro)vascular contributions to cognitive impairment and dementia (VCID) in aging cannot be overemphasized, and the pathogenesis and prevention of age-related cerebromicrovascular pathologies are a subject of intensive research. 4 key findings →
Evidence: low
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Inflammation is a complex biological response fundamental to how the body deals with injury and infection to eliminate the initial cause of cell injury and effect repair. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The blood-brain barrier (BBB) is a tightly regulated interface in the Central Nervous System (CNS) that regulates the exchange of molecules in and out from the brain thus maintaining the CNS homeostasis. 4 key findings →
Evidence: low
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Microglia are resident macrophages of the CNS that are involved in its development, homeostasis and response to infection and damage. 4 key findings →
Evidence: low
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Age is characterized by chronic inflammation, leading to synaptic dysfunction and dementia because the clearance of protein waste is reduced. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Parkinson's disease (PD) is the most common movement disorder. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
As the primary immune response cell in the central nervous system, microglia constantly monitor the microenvironment and respond rapidly to stress, infection, and injury, making them important modulators of neuroinflammatory responses. 4 key findings →
Evidence: low
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Myeloperoxidase, a heme protein expressed by professional phagocytic cells, generates an array of oxidants which are proposed to contribute to tissue damage during inflammation. 4 key findings →
Evidence: low
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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 →