Increasing evidence suggests that vascular risk factors contribute to neurodegeneration, cognitive impairment and dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Diffuse axonal injury after traumatic brain injury (TBI) produces neurological impairment by disconnecting brain networks. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
47/100
Cognitively normal subjects with HTN (n=19) had decreased rCBF in the putamen, globus pallidus, bilaterally, and in the left hippocampus compared with normotensives (n=22). 1 key finding →
Participants: 19 Evidence: low
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Microglial MVs are neurotoxic and myelinotoxic in the presence of Aβ1-42 . 4 key findings →
Evidence: low
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Sepsis is a major cause of death in intensive care units worldwide. 1 key finding →
Evidence: low
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Human immunodeficiency virus type 1 (HIV-1) infects the brains of a majority of patients with the acquired immunodeficiency syndrome (AIDS), and has been linked to the development of a progressive dementia termed "HIV-associated dementia." 4 key findings →
Evidence: low
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The results confirm that unilateral parkinsonism unresponsive to levodopa and limb ideomotor apraxia are the clinical hallmarks of corticobasal degeneration, and only a minority of patients with corticobasal degeneration present with dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
IL-6 levels were negatively associated with performance on the MMSE in this multiethnic cohort. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Recent literature has pointed to the existence of inflammasome-mediated inflammatory pathways in central nervous system (CNS) disorders and associated changes in behavior. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Chronic cerebral hypoperfusion has been associated with cognitive decline in aging and Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
47/100
Accumulation of amyloid-β in cerebral blood vessels occurs in familial and sporadic forms of cerebral amyloid angiopathy and is a prominent feature of Alzheimer disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Foam cells play a vital role in the initiation and development of atherosclerosis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Current brain spheroids or organoids derived from human induced pluripotent stem cells (hiPSCs) still lack a microglia component, the resident immune cells in the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Age-associated microglial dysfunction contributes to the accumulation of amyloid-β (Aβ) plaques in Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Eleven patients with idiopathic normal pressure hydrocephalus (NPH) were selected from an initial cohort of 43 patients. 4 key findings →
Participants: 43 Evidence: moderate
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Cholesteryl ester transfer protein inhibition (CETP) has been shown to increase levels of high-density lipoprotein cholesterol (HDL-C) and reduce levels of low-density lipoprotein cholesterol (LDL-C). 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebrovascular disease and Alzheimer disease are common diseases of aging and frequently coexist in the same brain. 4 key findings →
Evidence: low
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Amyloid deposition can take place in the walls of arteries, arterioles, and, less often, capillaries and veins of the central nervous system, a phenomenon known as cerebral amyloid angiopathy (CAA). 4 key findings →
Evidence: low
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An inflammatory process in the central nervous system (CNS) is believed to play an important role in the pathway leading to neuronal cell death in a number of neurodegenerative diseases including Parkinson's disease, Alzheimer's disease, prion diseases, multiple sclerosis and HIV-dementia. 4 key findings →
Evidence: low
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Traumatic brain injury (TBI) represents a major cause of death and disability in developed countries. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
47/100
Astrocyte infection with human immunodeficiency virus (HIV) is considered rare, so astrocytes are thought to play a secondary role in HIV neuropathogenesis. 3 key findings →
Evidence: low
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The world's population is steadily ageing and as a result, health conditions related to ageing, such as dementia, have become a major public health concern. 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
Though cerebral white matter injury is a frequently described phenomenon in aging and dementia, the cause of white matter lesions has not been conclusively determined. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the LA cohort only, higher WMHs load was associated with greater GM atrophy across all groups (HCs, AD, bvFTD), with a specific neurodegenerative pattern involving orbitofrontal, cingulate, and temporal areas. 5 key findings →
Participants: 402 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
10 of the 903 studies in this tag, 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.
- Relationship between ApoE, MRI findings, and cognitive function in the Cardiovascular Health Study
- Alzheimer's disease comorbidity in normal pressure hydrocephalus: prevalence and shunt response
- White matter hyperintensities, cognitive impairment and dementia: an update
- The burden of stroke, ischaemic heart disease, and dementia in Africa, 1990–2021: an ecological analysis of the Global Burden of Disease 2021
- White matter hyperintensities and imaging patterns of brain ageing in the general population
- Studying ventricular abnormalities in mild cognitive impairment with hyperbolic Ricci flow and tensor-based morphometry
- Hypertension, brain damage and cognitive decline
- Modes of covariation between vascular risk factors and cognition in cohorts with cultural and geographical variations
- Retinal vascular reactivity is associated with white matter hyperintensities and dysfunctional cerebrovascular reactivity in cerebral small vessel disease
- Vascular risk factors, large-artery atheroma, and brain white matter hyperintensities
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →