Blood-brain barrier (BBB) dysfunction might be an important component of many neurodegenerative disorders. 3 key findings →
Participants: 1,015 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Magnetic resonance-guided focused ultrasound in combination with intravenously injected microbubbles has been shown to transiently open the blood-brain barrier, and reduce beta-amyloid and tau pathology in animal models of Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The glymphatic movement of fluid through the brain removes metabolic waste 1-4 . 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
FUS-enhanced delivery of AAV resulted in a 12.6% knockdown of APOE ε4 gene expression in the targeted hippocampus, accompanied by an over 20% decrease in apoE4 protein levels and significant reductions in astrocyte and microglia levels. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This editorial summarizes advances from the Clearance of Interstitial Fluid and Cerebrospinal Fluid (CLIC) group, within the Vascular Professional Interest Area (PIA) of the Alzheimer's Association International Society to Advance Alzheimer's Research and Treatment (ISTAART). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
48/100
Cerebral amyloid angiopathy (CAA) is a small vessel disease characterized by the deposition of amyloid-beta in small cerebral vessels, which can lead to intracerebral hemorrhages and cognitive impairment. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
48/100
When risk factor p-values were FDR-adjusted, diastolic blood pressure was significantly associated with mean perfusion. 5 key findings →
Participants: 330 Evidence: low
Full summary, score breakdown and related studies → Original source
We included 110 patients with CAA (strictly lobar ICHs/CMBs), 33 with HA (strictly deep ICHs/CMBs) and 97 with mixed lobar/deep ICHs/CMBs. 5 key findings →
Participants: 110 Evidence: low
Full summary, score breakdown and related studies → Original source
Consistently lower Kw was evident across the AD continuum and may act as a diagnostic tool for early AD screening. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular contributions to cognitive impairment are increasingly recognized 1-5 as shown by neuropathological 6,7 , neuroimaging 4,8-11 , and cerebrospinal fluid biomarker 4,12 studies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ageing is a major risk factor for many neurological pathologies, but its mechanisms remain unclear. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Monoclonal antibodies targeting amyloid-β are the first approved disease-modifying treatment for Alzheimer’s disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The 88 patients with AD included 15 with microbleeds only in cortical/subcortical regions (cortical microbleeds) that could be CAA-related, 16 with microbleeds only in deep locations (deep microbleeds), 3 with microbleeds in both cortical and deep locations (mixed microbleeds), and 54 without microbleeds. 4 key findings →
Participants: 88 Evidence: low
Full summary, score breakdown and related studies → Original source
AD mice showed early decreases in NVC and bilateral connectivity (BC) in motor and cingulate cortex, and hypoconnectivity within the sensory-motor network. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy-related inflammation (CAA-RI) is an encephalopathy caused by inflammation of β-amyloid peptide deposition in cerebrovascular vessels. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is widely recognized as a multifactorial disorder involving neurovascular and glial dysfunction beyond amyloid-β and tau pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The human brain vasculature is of great medical importance: its dysfunction causes disability and death 1 , and the specialized structure it forms-the blood-brain barrier-impedes the treatment of nearly all brain disorders 2,3 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Macrophages are important players in the maintenance of tissue homeostasis 1 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our study has established a significant link between CAA-Aβ antibody immune complex formation, immune activation and vascular damage leading to smooth muscle cell loss. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) is a cerebrovascular disease characterized by vascular amyloid-β (Aβ) deposition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
The prevalence of cerebral amyloid angiopathy (CAA) has been shown to increase with age, with rates reported to be around 50-60% in individuals over 80 years old who have cognitive impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The adult quiescent blood-brain barrier (BBB), a structure organised by endothelial cells through interactions with pericytes, astrocytes, neurons and microglia in the neurovascular unit, is highly regulated but fragile at the same time. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The breath-holding index was reduced in the AD continuum and was inversely correlated to CSF amyloid β42 levels. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our analyses demonstrate lower retinal capillary densities in early disease, in cognitively normal APOE ε4 gene carriers. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) is an important cerebral small vessel disease associated with brain haemorrhage and cognitive change. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 247 studies in this tag that have a study page, 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.
- Oligodendrocyte stress response as a driver of vascular dementia
- Intravenous anti-Aβ immunotherapy acutely increases cerebral amyloid angiopathy and vascular damages in APOE4 mice
- Transcriptomic Profile of Blood-Brain Barrier Remodeling in Cerebral Amyloid Angiopathy
- Blood-Brain Barrier: From Physiology to Disease and Back
- Neurovascular dysfunction and vascular amyloid accumulation as early events in Alzheimer's disease
- MicroRNA-Mediated Therapy Modulating Blood-Brain Barrier Disruption Improves Vascular Cognitive Impairment
- Hypertension-Induced Cerebral Small Vessel Disease Leading to Cognitive Impairment
- Monogenic causes of cerebral small vessel disease and stroke
- Cerebral autoregulation, beta amyloid, and white matter hyperintensities are interrelated
- A brief overview of a mouse model of cerebral hypoperfusion by bilateral carotid artery stenosis
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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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