At autopsy the striatal dopaminergic transporter is reduced. 4 key findings →
Design: cohort study Evidence: moderate
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28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
At autopsy the striatal dopaminergic transporter is reduced. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
We examined whether sarcopenia is associated with the occurrence of late-life cognitive impairment. 4 key findings →
Participants: 1,175 Evidence: low
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
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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
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Among 8.5 million hospitalized patients aged 50 years or older, 2,335 had CAA and 600,646 had other CVDs. 5 key findings →
Design: cohort study Participants: 34 Evidence: moderate
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The aetiology of HS-A is heterogeneous, but HS-A is strongly associated with limbic-predominant age-related TDP-43 encephalopathy NC (LATE-NC). 5 key findings →
Participants: 1,933 Evidence: low
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Of 10 974 participants (60.0% female, mean [SD] age: 73.2 [6.8] years), 2445 developed incident all-cause dementia over 116 067 person-years of follow-up. 5 key findings →
Participants: 974 Evidence: moderate
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This study traces the course of pathology in incidental and symptomatic Parkinson cases and proposes a staging procedure based upon the readily recognizable topographical extent of the lesions. 3 key findings →
Evidence: low
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Infection with human immunodeficiency virus type 1 (HIV-1) is frequently complicated in its late stages by the AIDS dementia complex, a neurological syndrome characterized by abnormalities in cognition, motor performance, and behavior. 4 key findings →
Evidence: low
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The shared role of amyloid-β (Aβ) deposition in cerebral amyloid angiopathy (CAA) and Alzheimer disease (AD) is arguably the clearest instance of crosstalk between neurodegenerative and cerebrovascular processes. 4 key findings →
Evidence: low
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Mitochondria and the endoplasmic reticulum (ER) form tight structural associations and these facilitate a number of cellular functions. 4 key findings →
Evidence: low
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Cerebral amyloid angiopathy (CAA) results from deposition of β-amyloid in the media and adventitia of small arteries and capillaries of the leptomeninges and cerebral cortex and is a major cause of lobar intracerebral hemorrhage and cognitive impairment in the elderly. 3 key findings →
Evidence: low
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We studied the frequency, severity, and clinical correlations of cerebral amyloid angiopathy (CAA) in 117 CERAD subjects with autopsy-confirmed AD. 4 key findings →
Evidence: low
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Alzheimer's disease, a fatal neurodegenerative disorder of unknown aetiology, is usually considered to be a single disorder because of the general uniformity of the disease phenotype. 4 key findings →
Evidence: low
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With advances in healthcare and an ageing population, the number of older adults with epilepsy is set to rise substantially across the world. 4 key findings →
Evidence: low
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Mutations in presenilin 2 are rare causes of early onset familial Alzheimer's disease. 4 key findings →
Participants: 64 Evidence: low
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In frontotemporal dementia and amyotrophic lateral sclerosis, the RNA-binding protein TDP-43 is depleted from the nucleus of neurons in the brain and spinal cord. 2 key findings →
Evidence: low
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Chronological age is an imperfect estimate of molecular aging. 5 key findings →
Participants: 4,018 Evidence: low
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Based on data from their first NACC visit with AD, there was considerable heterogeneity in language performance across people with EOAD and LOAD. 5 key findings →
Design: cross-sectional Participants: 1,189 Evidence: low
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The study sample included 3566 Black (16 104 observations) and 17 555 White (90 874 observations) participants. 5 key findings →
Design: cross-sectional Participants: 3,566 Evidence: low
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Elaborating on the results, we validated one finding using a quantitative assessment of TDP-43 pathology in the granular layer of the hippocampus in FTLD-TDP brain donors with (n = 15) and without (n = 15) hallucinations. 3 key findings →
Participants: 15 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma phospho-tau217 correlated with plasma phospho-tau181, CSF phospho-tau217 (rs = 0.68, P < 0.001), and negatively with CSF β-amyloid42/40 (rs = -0.52, P = 0.001). 4 key findings →
Design: cross-sectional Participants: 35 Evidence: low
Full summary, score breakdown and related studies → Original source
A diagnostic rubric is required to distinguish between limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) and frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP). 3 key findings →
Participants: 514 Evidence: low
Full summary, score breakdown and related studies → Original source
TDP-43 was significantly elevated in plasma ADEVs derived from autopsy confirmed LATE-NC subjects, with or without comorbid AD pathology. 4 key findings →
Participants: 22 Evidence: moderate
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 (3.7% 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 →