Neuroinflammation is considered one of major factors in the pathogenesis of Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The advent of high-throughput 'omics' technologies has improved our knowledge of gut microbiome in human health and disease, including Alzheimer's disease (AD), a neurodegenerative disorder. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The gut-brain axis refers to the bidirectional communication between the gut and brain, and regulates intestinal homeostasis and the central nervous system via neural networks and neuroendocrine, immune, and inflammatory pathways. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The microbiota-gut-brain axis refers to the intricate bidirectional communication between commensal microorganisms residing in the digestive tract and the central nervous system, along neuroendocrine, metabolic, immune, and inflammatory pathways. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common type of dementia in the elderly and causes neurodegeneration, leading to memory loss, behavioral disorder, and psychiatric impairment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral endothelial cells and their linking tight junctions form a unique, dynamic and multi-functional interface, the blood-brain barrier (BBB). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease (CSVD) represents a diverse cluster of cerebrovascular diseases primarily affecting small arteries, capillaries, arterioles and venules. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
α-syn aggregates represent the pathological hallmark of synucleinopathies as well as a frequent copathology (almost 1/3 of cases) in AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The development of new therapeutic avenues that target the early stages of Alzheimer's disease (AD) is urgently necessary. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Alzheimer's disease (AD) is the main cause of dementia worldwide. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
P021 treatment during early development prevented cognitive impairment and increased expressions of pCREB and BDNF that activated downstream various signaling cascades such as PLC/PKC, MEK/ERK and PI3K/Akt, and ameliorated synaptic protein deficit in 4-month-old 3xTg-AD mice. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mechanisms of protein homeostasis are crucial for overseeing the clearance of misfolded and toxic proteins over the lifetime of an organism, thereby ensuring the health of neurons and other cells of the central nervous system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
TCM could modulate signal pathways related to AD pathological progression, including NF-κB, Nrf2, JAK/STAT, ubiquitin-proteasome pathway, autophagy-lysosome pathway-related AMPK/mTOR, GSK-3/mTOR, and PI3K/Akt/mTOR, as well as SIRT1 and PPARα pathway. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aging is a major risk factor for many age-associated disorders, including neurodegenerative diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the accumulation of misfolded amyloid-beta and tau proteins. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases (ND) pose a serious health burden to society and healthcare systems alike, with increasing incidence rates especially within aging populations. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases (NDs) are characteristic with progression of neuron degeneration, resulting in dysfunction of cognition and mobility. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Abnormal accumulation of misfolded proteins in the endoplasmic reticulum and their aggregation causes inflammation and endoplasmic reticulum stress. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Patients with mild AD had higher total costs, patient medical costs, patient social care costs, and family caregiver informal care costs than did patients with MCI; however, only patient medical costs were significantly different (p = 0.022). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A formal evaluation of the health equity impact of a new intervention is hardly ever performed as part of a health technology assessment to understand its value. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Under the initial assumption that the hypothetical gene therapy grants a 30% risk reduction in disease progression and entry into institutional care, the maximum cost-effective price for gene therapy is $141,126 per treatment using the threshold of $150,000 per quality-adjusted life year (QALY). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Anti-amyloid antibody treatment for Alzheimer’s disease is linked to Amyloid-Related Imaging Abnormalities (ARIA), including vasogenic edema (ARIA-E) and microhemorrhages (ARIA-H), especially in ApoE ε4/4 carriers. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Considering the overall sci-entific evidence presented, it is important to note that GLPs are no longer just antihyperglycemic drugs but are remarkably versatile, with a future in almost every field of medicine. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This case underscores the importance of routine sodium monitoring in elderly patients with dementia initiated on serotonergic or antipsychotic therapy. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The results of the aducanumab studies have not been published in peer-reviewed form and both the analysis presented by Dr Knopman and collaborators and this perspective are based on data presented in 2019 at the Clinical Trials in AD (CTAD) meeting3; both discussions must be seen as tentative until full data are available. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 3,071 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.
- Application of P7C3 Compounds to Investigating and Treating Acute and Chronic Traumatic Brain Injury
- Targeting redox imbalance in neurodegeneration: characterizing the role of GLP-1 receptor agonists
- Chronic lithium administration to FTDP-17 tau and GSK-3beta overexpressing mice prevents tau hyperphosphorylation and neurofibrillary tangle formation, but pre-formed neurofibrillary tangles do not revert
- Tango-therapy vs physical exercise in older people with dementia; a randomized controlled trial
- Discovering and targeting the basic mechanism of neurodegeneration: the role of peptides from the C-terminus of acetylcholinesterase: non-hydrolytic effects of ache: the actions of peptides derived from the C-terminal and their relevance to neurodegeneration
- European Stroke Organisation and European Academy of Neurology joint guidelines on post-stroke cognitive impairment
- Curcumin Modulation of the Gut-Brain Axis for Neuroinflammation and Metabolic Disorders Prevention and Treatment
- Transcriptomic Analysis in the Hippocampus and Retina of Tg2576 AD Mice Reveals Defective Mitochondrial Oxidative Phosphorylation and Recovery by Tau 12A12mAb Treatment
- Comparing ARIA-E severity scales and effects of treatment management thresholds
- Effect of Cholinesterase Inhibitors on Mortality in Patients With Dementia: A Systematic Review of Randomized and Nonrandomized Trials
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →