Aggregation of amyloid-β (Aβ) peptides leads to synaptic disruption and neurodegeneration in Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Allelic variation in the apolipoprotein E (APOE) gene is the major risk factor of sporadic Alzheimer disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the leading cause of dementia worldwide. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E (apoE), a chaperone for the amyloid beta (Abeta) peptide, regulates the deposition and structure of Abeta that deposits in the brain in Alzheimer disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The term "aging-related tau astrogliopathy" (ARTAG) describes pathological accumulation of abnormally phosphorylated tau protein in astrocytes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
47/100
The ATP-binding cassette transporter A7 (ABCA7) has been identified as a susceptibility factor of late onset Alzheimer disease in genome-wide association studies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
APOE-epsilon4 is associated with small vessel arteriolosclerosis, microinfarcts of the deep nuclei, neuritic senile plaque density, and amyloid angiopathy in patients with autopsy-proven Alzheimer disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
These CSF A beta 42 findings are consistent with acceleration by the APOE*4 allele of pathogenic A beta 42 brain deposition starting in later middle age in persons with normal cognition. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Among 124 876 cases and controls, genome-wide conjunction analyses of ALS, FTD, PD, AD, CBD, and PSP revealed significant genetic overlap between ALS and FTD at known ALS loci: rs13302855 and rs3849942 (nearest gene, C9orf72; P = .03 for rs13302855 and P = .005 for rs3849942) and rs4239633 (nearest gene, UNC13A; P = .03). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most common form of dementia and it is characterized by the deposition of amyloid-β (Aβ) plaques and neurofibrillary tangles in the brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
47/100
Age-associated dementia and Alzheimer's disease (AD) are currently epidemic. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Accumulating studies suggest that overnutrition-associated obesity may lead to development of type 2 diabetes mellitus and metabolic syndromes (MetS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Although amyloid plaques and neurofibrillary pathology play important roles in Alzheimer disease (AD), our understanding of AD is incomplete, and the contribution of microglia and iron to neurodegeneration is unknown. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is the leading cause of dementia in the elderly and is defined by two pathological hallmarks; the accumulation of aggregated amyloid beta and excessively phosphorylated Tau proteins. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Multiple different pathological protein aggregates are frequently seen in human postmortem brains and hence mixed pathology is common. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuroprotection alone is not sufficient to rescue tau-induced memory loss in a transgenic mouse model. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Human immunodeficiency virus type 1 (HIV-1) infects the brains of a majority of patients with the acquired immunodeficiency syndrome (AIDS), and has been linked to the development of a progressive dementia termed "HIV-associated dementia." 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The results confirm that unilateral parkinsonism unresponsive to levodopa and limb ideomotor apraxia are the clinical hallmarks of corticobasal degeneration, and only a minority of patients with corticobasal degeneration present with dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We conclude that variations in morphologies among microglial cells, and cells of macrophage lineage, can help guide future work connecting neuroinflammatory mechanisms with specific neurodegenerative disease subtypes. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is the most common form of dementia among the elderly and is characterized by progressive loss of memory and cognition. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent literature has pointed to the existence of inflammasome-mediated inflammatory pathways in central nervous system (CNS) disorders and associated changes in behavior. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
AD, DS, and DSAD brains also have reduced mtDNA ND6 mRNA levels, altered mtDNA copy number, and perturbed Aβ metabolism. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Down syndrome (DS) is the result of triplication of chromosome 21 (trisomy 21) and is the prevailing cause of mental retardation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Genetic variations in promoter sequences that alter gene expression play a prominent role in increasing susceptibility to complex diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There is convincing epidemiological and in vitro evidence of chronic oxidative stress in individuals with Down syndrome (DS). 5 key findings →
Participants: 166 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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.
- Longitudinal 18F-MK-6240 tau tangles accumulation follows Braak stages
- Beta-amyloid imaging and memory in non-demented individuals: evidence for preclinical Alzheimer's disease
- RNA Oxidation Is a Prominent Feature of Vulnerable Neurons in Alzheimer’s Disease
- Age-dependent instability of mature neuronal fate in induced neurons from Alzheimer's patients
- The contribution of astrocytes and microglia to traumatic brain injury
- Human immunodeficiency virus encephalitis in SCID mice
- Interactions of pathological proteins in neurodegenerative diseases
- The role of tau in the pathological process and clinical expression of Huntington's disease
- Identification and cloning of human astrocyte genes displaying elevated expression after infection with HIV-1 or exposure to HIV-1 envelope glycoprotein by rapid subtraction hybridization, RaSH
- Inhibition of IL-12/IL-23 signaling reduces Alzheimer's disease-like pathology and cognitive decline
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 →