Alzheimer's disease (AD) is the most prevalent dementia, affecting a large number of populations. 4 key findings →
Evidence: low
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Research
29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer disease (AD) and epilepsy are major causes of neurologic disability and are reciprocally related: epileptiform discharges, subclinical seizures, and epilepsy are more prevalent in patients with AD compared with controls; progressive cognitive impairment commonly afflicts epilepsy patients; and late-onset epilepsy patients have higher rates of new-onset dementia. 4 key findings →
Evidence: low
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Lesions of Alzheimer disease are associated with low-grade but sustained inflammatory responses. 4 key findings →
Evidence: low
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Microglia, residential macrophages in the central nervous system, can release a variety of factors including cytokines, chemokines, etc. to regulate the communication among neuronal and other types of glial cells. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Alzheimer type II astrocyte change is the distinctive morphologic alteration in brain of humans and experimental animals succumbing to hepatic encephalopathy (HE). 4 key findings →
Evidence: low
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Cytoskeletal abnormalities and synaptic loss, typical of both familial and sporadic Alzheimer disease (AD), are induced by diverse stresses such as neuroinflammation, oxidative stress, and energetic stress, each of which may be initiated or enhanced by proinflammatory cytokines or amyloid-β (Aβ) peptides. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) diagnosis is confirmed using a medley of modalities, such as the detection of amyloid-β (Aβ) neuritic plaques and neurofibrillary tangles with positron electron tomography (PET) or the appraisal of irregularities in cognitive function with examinations. 3 key findings →
Participants: 53 Evidence: low
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We observed that GSK-3β activity was significantly upregulated in ApoE4 mice, accompanied by disruption of the insulin signaling pathway. 5 key findings →
Evidence: low
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In analyses of APOE ε4 carriers, dosage, and genetic risk score, APOE ε4 was associated with lower odds of fluctuating cognition and parkinsonism and higher odds of visual hallucinations. 5 key findings →
Evidence: low
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There is significant evidence that microglia contribute to neuroinflammation and neurotoxicity in AD 1,2 , yet there is also evidence to the contrary. 5 key findings →
Participants: 89 Evidence: low
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Although β-site APP-cleaving enzyme 1 (BACE1) and secretase inhibitors did not achieve success in clinical trials because of mechanism-based toxicity and cognitive impairment, new monoclonal antibodies such as lecanemab and donanemab have shown high amyloid plaque clearance and reduced cognitive deterioration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer′s disease (AD) is a chronic neurodegenerative disorder that leads to memory loss and changes in mental and behavioral functions in elderly individuals. 4 key findings →
Evidence: low
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Alzheimer’s disease (AD) is a progressive neurodegenerative disorder marked by memory loss, cognitive decline, and behavioral changes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Brain functional connectivity alterations, that is, pathological changes in the signal exchange between areas of the brain, are occurring in several neurological diseases, including neurodegenerative and neuropsychiatric ones. 5 key findings →
Evidence: low
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Understanding the distribution of SV2A in DS will provide insight on changes to synaptic density in populations with accelerated AD neuropathology. 3 key findings →
Participants: 94 Evidence: moderate
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Understanding the distribution of SV2A in DS will provide insight on changes to synaptic density in populations with accelerated AD neuropathology. 3 key findings →
Participants: 94 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer’s disease is the most common type of dementia, characterized by a progressive decline in cognitive function, particularly memory and impacting daily life. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Existing models of frontotemporal dementia (FTD) may not fully recapitulate the pathophysiology of the disease. 1 key finding →
Evidence: low
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Lewy bodies and neurofibrillary tangles, composed of α-synuclein (α-syn) and tau, respectively, often are found together in the same brain and correlate with worsening cognition. 3 key findings →
Evidence: low
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Tau mutant cortical organoids showed altered mitochondrial function and gene expression related to neuronal development, with synaptic markers and neuronal activity reduction. 5 key findings →
Evidence: low
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Mild cognitive impairment (MCI) and sarcopenia are prevalent age-related conditions that often coexist and share common mechanisms such as chronic inflammation, reduced neuroplasticity, and impaired muscle function. 1 key finding →
Design: narrative review Evidence: low
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Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease without effective treatments. 1 Extracellular amyloid plaques, neurofibrillary tangles, neuroinflammation, and neuronal loss are the characteristics of AD neuropathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In previous studies, we isolated a series of novel gentisides with nerve growth factor (NGF)-mimic activities from Gentiana rigescens Franch and conducted continuous structure–activity relationship (SAR) studies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
39/100
The repeated inability of Aβ therapies to pass clinical tests in sporadic AD points to the complexity of the disease and indicates that earlier or more interventions could be necessary. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The human brain is one of the most metabolically active tissues in the body, due in large part to the activity of trillions of synaptic connections. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 8,203 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.
- Amyloid-β (Aβ) immunotherapy induced microhemorrhages are associated with activated perivascular macrophages and peripheral monocyte recruitment in Alzheimer's disease mice
- Cerebral Microbleeds Are Associated with Cerebral Hypoperfusion in Patients with Alzheimer's Disease
- Modification of the relationship of the apolipoprotein E ε4 allele to the risk of Alzheimer disease and neurofibrillary tangle density by sleep
- Oligodendrocyte Enriched Brain Organoids Reveal Impaired Oligodendroglial Maturation and Altered Neural Network Activity in Down Syndrome
- REST and stress resistance in ageing and Alzheimer's disease
- Vascular amyloid alters astrocytic water and potassium channels in mouse models and humans with Alzheimer's disease
- Enduring cognitive, neurobehavioral and histopathological changes persist for up to one year following severe experimental brain injury in rats
- Diet and Alzheimer's dementia - Nutritional approach to modulate inflammation
- Amyloid PET Ligands for Dementia
- Local externalization of phosphatidylserine mediates developmental synaptic pruning by microglia
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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →