Significant progress has been made in understanding the pre-symptomatic phase of amyotrophic lateral sclerosis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Significant progress has been made in understanding the pre-symptomatic phase of amyotrophic lateral sclerosis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In Alzheimer disease (AD), amyloid β peptide (Aβ) accumulates in plaques in the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study aimed to identify lipid species associated with MPH response and explore lipid pathway disruptions in responders versus non-responders. 3 key findings →
Design: randomized controlled trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Baseline data of 423 PD patients and 196 HCs yielded no between-group differences in demographic characteristics. 3 key findings →
Evidence: moderate
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Vascular dysfunction has a critical role in Alzheimer's disease (AD). 4 key findings →
Evidence: low
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During the COVID-19 pandemic, home health agencies (HHAs) discharges following acute hospitalizations increased. 1 key finding →
Design: cohort study Participants: 426,766 Evidence: moderate
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The results showed that 68.02% of caregivers were highly burdened and 65% exhibited depressive symptoms. 3 key findings →
Evidence: low
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In the ADMET2 biomarker subset (n = 44, MPH:21, age:75 years, MMSE:20.2), higher baseline TNF was associated with higher M6 NPI-A [B(SE)= 6.86 (1.71), p = .0003], and multivariable models found lower baseline TNF [B(SE)= 8.28(1.61), p < .001] and higher baseline S100B [B(SE)= -6.41(1.95), p = .002] were associated with lower M6 NPI-A. Exploratory analyses suggested that higher baseline NfL significantly interacted with treatment to predict lower M6 NPI-A [B(SE)= -8.36(4.21), p = .05], only when adjusting for cognition. 5 key findings →
Participants: 44 Evidence: high
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The VSOP/A group had significantly improved processing speed and attention performance compared to the VE group, and these differences persisted through 6 months postintervention. 4 key findings →
Design: randomized controlled trial Evidence: high
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The objective of this study was to describe the occurrence of HIV dementia and neuropsychological testing abnormalities in a new cohort of HIV-seropositive individuals at high risk for HIV dementia and to compare these results to a cohort before the advent of highly active antiretroviral therapy (HAART). 2 key findings →
Evidence: moderate
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Elevation of the proinflammatory cytokine Interleukin-1 (IL-1) is an integral part of the local tissue reaction to central nervous system (CNS) insult. 4 key findings →
Evidence: low
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The study cohort included 1 415 265 long-stay nursing home residents with dementia who died between 2013 and 2022. 5 key findings →
Design: cohort study Evidence: moderate
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Considerable variations of breadth and intensity in county-level HCBS were observed. 4 key findings →
Participants: 365,310 Evidence: low
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SNF discharges decreased while home and HHA discharges increased during the pandemic. 5 key findings →
Participants: 830,656 Evidence: moderate
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[(11)C]-Pittsburgh Compound B (PIB) PET is specific for fibrillar Abeta molecular pathology but not for pathologic diagnosis of comorbid Alzheimer disease in individuals with Parkinson disease dementia. 1 key finding →
Evidence: low
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Neuroinflammation is critically involved in numerous neurodegenerative diseases, and key signaling steps of innate immune activation hence represent promising therapeutic targets. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuroinflammation is a conspicuous feature of Alzheimer disease (AD) pathology and is thought to contribute to the ultimate neurodegeneration that ensues. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microinfarcts occur commonly in the aging brain as a consequence of diffuse embolic events and are associated with the development of vascular dementia and Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuroinflammation is considered one of the cardinal features of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Caring for elderly people with dementia is associated with well-documented increases in burden, distress, and decrements in mental health and wellbeing. 2 key findings →
Evidence: low
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New personalized endpoints that are clinically meaningful to individuals and their families should be developed. 1 key finding →
Evidence: low
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Although epidemiological data associate hypertension with a strong predisposition to develop Alzheimer disease, no mechanistic explanation exists so far. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Accumulation of amyloid beta-peptide (Abeta) in the central nervous system (CNS) may initiate pathogenic cascades mediating neurovascular and neuronal dysfunctions associated with the development of cerebral beta-amyloidosis and cognitive decline in patients with Alzheimer disease (AD) and with related familial cerebrovascular disorders. 3 key findings →
Evidence: low
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Human immunodeficiency virus (HIV) infection is commonly associated with neurological disease that occurs in the apparent absence of extensive infection of brain cells by HIV, suggesting that indirect mechanisms account for neuropathogenesis in the CNS, perhaps including changes in the normal neuroprotective functions of astrocytes. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microinfarcts are a common clinical feature of the aging brain, particularly in patients with cognitive decline or vascular or Alzheimer's dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →