Cerebral amyloid angiopathy is diagnosed in stroke units after lobar intracerebral hemorrhage. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
In recent years, studies have demonstrated that hypertension-related changes (e.g., small vascular lesions, inflammatory reactions, hypoperfusion, oxidative stress, damage to autoregulatory processes and the blood-brain barrier, and cerebral amyloid angiopathy) can occur over time in cerebral small vessels, potentially leading to lower cognitive function when blood pressure (BP) control is poor or lacking. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
The number of microbleeds was significantly correlated with the severity of decrease in the occipital lobe (Spearman's r = 0.531, p < 0.001) and temporal lobe (r = 0.437, p < 0.001) but not in the frontal lobe (r = 0.201, p = 0.101) and parietal lobe (r = 0.178, p = 0.146). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Over the past decades, a frequent co-morbidity of cerebrovascular pathology and Alzheimer's disease has been observed. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Androgens affect the cerebral vasculature and may contribute to sex differences in cerebrovascular diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The prevalence of BMB is highly variable (3%-27% in the general population, 6%-80% in patients with vascular risk factors or vascular disease, and 16%-45% in patients with cognitive impairment). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sex differences exist in how cerebral blood vessels function under both physiological and pathological conditions, contributing to observed sex differences in risk and outcomes of cerebrovascular diseases (CBVDs), such as vascular contributions to cognitive impairment and dementia (VCID) and stroke. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
Our data suggests that microglial reactivity may play a role in hippocampal atrophy; potentially contributing to the increasingly recognized interaction between vascular and neurodegenerative pathology. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Poststroke cognitive impairment (PSCI) refers to any level of cognitive decline occurring after a stroke, ranging from mild to severe impairments, while PSCI with dementia describes a more severe form where the cognitive decline significantly affects daily functioning and meets the clinical criteria for dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
For women who initiate HT more than 10 or 20 years from menopause onset or are aged 60 years or older, the benefit-risk ratio appears less favorable because of the greater absolute risks of coronary heart disease, stroke, venous thromboembolism, and dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease (SVD) is commonly observed on neuroimaging among elderly individuals and is recognized as a major vascular contributor to dementia, cognitive decline, gait impairment, mood disturbance and stroke. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Brain photobiomodulation (PBM) therapy using red to near-infrared (NIR) light is an innovative treatment for a wide range of neurological and psychological conditions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Small vessel diseases (SVDs) are a group of disorders that result from pathological alteration of the small blood vessels in the brain, including the small arteries, capillaries and veins. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The critical role of the vasculature and its repair in neurological disease states is beginning to emerge particularly for stroke, dementia, epilepsy, Parkinson's disease, tumors and others. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
With increase in life expectancy, the number of persons suffering from common age-related brain diseases, including neurodegenerative (e.g., dementia) and cerebrovascular (e.g., stroke) disease is expected to rise substantially. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hypertension is a leading cause of stroke and dementia, effects attributed to disrupting delivery of blood flow to the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia is a major social and economic problem for our aging population. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The blood-brain barrier (BBB) prevents neurotoxic plasma components, blood cells, and pathogens from entering the brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The blood-brain barrier (BBB) plays a key role in maintaining the specialized microenvironment of the central nervous system (CNS), and enabling communication with the systemic compartment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Paravascular drainage of solutes, including β-amyloid (Aβ), appears to be an important process in brain health and diseases such as Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
The aim of this report was to describe the case of an elderly patient with cerebral amyloid angiopathy and associated dementia who presented with new onset symptomatology compatible with an acute cerebrovascular event. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) is characterized by amyloid deposition in cortical and leptomeningeal vessels. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aging influences cerebrovascular disease expression by a variety of mechanisms. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Emerging studies link vascular risk factors and cerebrovascular health to the prevalence and rates of progression in Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular risk factors and cerebrovascular disease are common causes of dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events