Alzheimer's disease (AD) is the most common cause of dementia in the general population and, to date, constitutes a major therapeutic challenge. 2 key findings →
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.
Recent studies showed increased expression of complements in various neurodegenerative diseases, including Alzheimer's and Parkinson's diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The prevalence of neurodegenerative disease has increased significantly in recent years, and with a rapidly aging global population, this trend is expected to continue. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Alzheimer's disease (AD) is a neurodegenerative disorder with no clear causative event making the disease difficult to diagnose and treat. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Alzheimer's disease (AD) is the most common progressive neurodegenerative disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The innate immune system plays key roles in controlling Alzheimer's disease (AD), while secreting cytokines to eliminate pathogens and regulating brain homeostasis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
To maintain homeostasis, an organism must detect and resolve sterile tissue damage. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the main cause of dementia worldwide. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Extensive human studies and animal models show that chronic immune system stimulation involving microglia, inflammasome, complement activation, synthesis of cytokines, and reactive oxygen species exacerbates neurodegeneration in Alzheimer's disease (AD) and other tauopathies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is an increasing prevalence of Vascular Cognitive Impairment (VCI) worldwide, and several studies have suggested that Chronic Cerebral Hypoperfusion (CCH) plays a critical role in disease onset and progression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Alzheimer's disease (AD), also known as senile dementia, is the most common degenerative disease of the central nervous system. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia, resident immune cells of the central nervous system (CNS), play a pivotal role in immune surveillance and maintenance of neuronal health. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid plaques are considered to be the pathological hallmark of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Parkinson's disease is characterized by accumulation of α-synuclein (αSyn). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia among several neurodegenerative disorders afflicting the elderly. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Inflammation plays important roles in the progress of neurodegenerative diseases, such as Parkinson's disease and Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuroinflammation is the fundamental immune response against multiple factors in the central nervous system and is characterized by the production of inflammatory mediators, activated microglia and astrocytes, and the recruitment of innate and adaptive immune cells to inflammatory sites, that contributes to the pathological process of related brain diseases, such as Alzheimer's disease, Parkinson's disease, depression, and stroke. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by memory loss and cognitive decline, is a major cause of death and disability among the older population. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Inflammasomes are intracellular protein complexes, members of the innate immune system, and their activation and regulation play an essential role in maintaining homeostatic conditions against exogenous and endogenous stimuli. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most prevalent cause of dementia worldwide. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The aim of this review is to explore the role of NLRP3 activation-mediated neuronal pyroptosis and neuroinflammation in neurodegenerative diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The autophagy-lysosomal pathway plays a critical role in intracellular clearance and metabolic homeostasis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The complement system is an ancient collection of proteolytic cascades with well-described roles in regulation of innate and adaptive immunity. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pathogenesis of neurodegenerative diseases involves the accumulation of misfolded protein aggregates. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A growing body of basic research has shown that EA can ameliorate neuroinflammation centrally (in animal models of ischemic stroke, Alzheimer's disease, traumatic brain injury, spinal cord injury, Parkinson's disease and vascular dementia) and peripherally (e.g. after a surgical insult or injection of lipopolysaccharide) and that its effects involve different molecular mechanisms, including activation of the α7 nicotinic acetylcholine receptor signaling pathway and P2 type purinergic receptors, inhibition of nuclear factor κB, and mitigation of damage secondary to oxidative stress and NOD-like receptor protein 3 inflammasome activation. 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 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 →