Aging is associated with chronic systemic inflammation, which contributes to the development of many age-related diseases, including vascular disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
These results suggest that persons carrying certain genotypes in IL10 (-1082G/A), IL1β (1473C/G), IL6 (-174C/G), and TNFIα (-308A/G) could be more vulnerable to development of neuroinflammation, and consequently of AD. 2 key findings →
Participants: 115 Evidence: low
Full summary, score breakdown and related studies → Original source
Experimental studies indicate that overactivation of the DNA repair protein poly(ADP-ribose) polymerase (PARP) in response to oxidative damage to DNA can cause cell death due to depletion of NAD+. 3 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
47/100
It is currently unclear how amyloid-β and tau deposition are linked to changes in synaptic function and axonal structure over the course of Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based tests have sparked tremendous attention in non-invasive early diagnosis of Alzheimer's disease (AD), a most prevalent neurodegenerative malady worldwide. 3 key findings →
Participants: 27 Evidence: low
Full summary, score breakdown and related studies → Original source
To determine whether apparent involvement of DYRK1A in Alzheimer's disease (AD) pathology makes it a candidate plasma biomarker for diagnosis, we developed a method to quantify plasma DYRK1A by immunoblot in transgenic mouse models having different gene dosages of Dyrk1a, and, consequently, different relative protein expression. 4 key findings →
Participants: 26 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
Vascular contributions to dementia and Alzheimer's disease are increasingly recognized 1-6 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
47/100
Defective brain hormonal signaling has been associated with Alzheimer's disease (AD), a disorder characterized by synapse and memory failure. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Air pollution is a serious environmental problem. 2 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
A mutation at codon 717 of the beta-amyloid precursor protein gene has been found to cosegregate with familial Alzheimer's disease in a single family. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Autophagy is markedly impaired in Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the selective vulnerability of specific neuronal populations, the molecular signatures of which are largely unknown. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Activation of microglia is a prominent pathological feature in tauopathies, including Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The role of microglia cells in Alzheimer's disease (AD) is well recognized, however their molecular and functional diversity remain unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
47/100
Previous studies have identified a crucial role of the gut microbiome in modifying Alzheimer's disease (AD) progression. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by synaptic loss, which can result from dysfunctional microglial phagocytosis and complement activation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The prefrontal cortex (PFC) serves as the chief executive officer of the brain, controlling the highest level cognitive and emotional processes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
[ 18 F]AV-1451 binds to tau in AD, and some other tauopathies. 2 key findings →
Participants: 33 Evidence: low
Full summary, score breakdown and related studies → Original source
There is a strong relationship between beta-amyloid deposition and atrophy very early in the disease process. 2 key findings →
Participants: 34 Evidence: low
Full summary, score breakdown and related studies → Original source
These results are supportive of an association between exercise engagement and AD biomarkers in cognitively normal older adults. 5 key findings →
Participants: 56 Evidence: low
Full summary, score breakdown and related studies → Original source
Antiamyloid antibodies have been used to reduce cerebral amyloid-beta (Aβ) load in patients with Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The amyloid hypothesis has been the dominant framework for Alzheimer's disease (AD) research, including the development of anti-AD therapies. 2 key findings →
Participants: 196 Evidence: low
Full summary, score breakdown and related studies → Original source
47/100
Amyloid-related imaging abnormalities (ARIA), side effects of anti-amyloid drugs seen in magnetic resonance imaging of the brain, are a major safety concern in patients with Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 6,970 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.
- Human microglial state dynamics in Alzheimer's disease progression
- Disentangling and quantifying the relative cognitive impact of concurrent mixed neurodegenerative pathologies
- Longitudinal change in CSF biomarkers in autosomal-dominant Alzheimer's disease
- The development and validation of tau PET tracers: current status and future directions
- Distinct dynamic profiles of microglial activation are associated with progression of Alzheimer's disease
- Intracerebroventricular streptozotocin impairs adult neurogenesis and cognitive functions via regulating neuroinflammation and insulin signaling in adult rats
- An NF-kappaB-sensitive micro RNA-146a-mediated inflammatory circuit in Alzheimer disease and in stressed human brain cells
- Age, neuropathology, and dementia
- Toward precision risk stratification of postoperative cognitive dysfunction: Preoperative inflammatory and neurodegenerative protein biomarkers in orthopedic surgery: A systematic review
- Perivascular drainage of amyloid-beta peptides from the brain and its failure in cerebral amyloid angiopathy and Alzheimer's disease
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →