Microglia have been identified as key players in Alzheimer's disease pathogenesis, and other neurodegenerative diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are neurodegenerative diseases with overlap in clinical presentation, neuropathology, and genetic underpinnings. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Of the 944 clinical cases, 13.0% were characterized as probable LATE (2.4% pure LATE and 10.6% LATE+AD) and 23.7% were characterized as probable AD without LATE. 5 key findings →
Participants: 944 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We analyzed data from 1,542 participants (mean age = 72.2 years, SD = 7.2; 50.8% female; mean education = 16.3 years, SD = 2.6) and found that APOE4 was associated with steeper declines in episodic memory as a function of Aβ duration. 5 key findings →
Participants: 1,542 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
46/100
An international expert panel convened to evaluate nutrition-based approaches to brain health and dementia prevention. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Converging evidence suggests that accumulation may be driven by spreading through network connections and/or interactions with amyloid-β (Aβ). 2 key findings →
Participants: 522 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In a heterogeneous autopsy sample, AD and LB pathology both contribute to cholinergic basal forebrain degeneration whereas hippocampus atrophy is more specifically related to AD pathology. 4 key findings →
Participants: 248 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Glymphatic activity in bvFTD correlated strongly with vascular dysfunction and astrocytic activation, and was associated with brain changes and clinical severity. 5 key findings →
Participants: 61 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Among 635 AD patients without LB, 62 (9.7%) presented parkinsonism, which correlated with reduced nigral neuron density (p < 0.01). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
GBA is the major risk gene for Parkinson’s disease (PD) and dementia with Lewy bodies (DLB), two common α-synucleinopathies with cognitive deficits. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 Free full text
Serum beta-synuclein level was progressively increased in the AD continuum across the preclinical, MCI and dementia stages compared with controls and was correlated with serum pTau181 (r=0.710), NfL (r=0.494) and GFAP concentrations (r=0.621, p<0.001 for all). 5 key findings →
Participants: 56 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
46/100
TDP-43_SAA was positive in 29/65 patients with sporadic MND, 9/21 patients with genetic MND, 6/17 OND patients and 3/22 controls. 5 key findings →
Participants: 65 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We found higher lipid droplet accumulation in primary fibroblasts derived from these mice, as well as in the brain of the mutant mice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is a progressive neurodegenerative disease marked by the accumulation of extracellular β-amyloid (Aβ) plaques and intracellular neurofibrillary tangles containing tau protein. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
46/100
The locus coeruleus (LC) is the source of norepinephrinergic innervation in the human brain. 2 key findings →
Participants: 134 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Neurodegenerative disorders alter mitochondrial functions, including the production of reactive oxygen species (ROS). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The maturation and stabilization of appropriate synaptic connections is a vital step in neural circuit development; however, the molecular signals underlying these processes are not fully understood. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Higher glial fibrillary acidic protein (GFAP) was associated with higher depressive symptoms. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a major public health concern in societies with increasingly ageing populations. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Genetic diversity in the apolipoprotein E (ApoE) gene has been identified as the major susceptibility genetic risk factor for sporadic Alzheimer’s disease (SAD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
ADAM10 is a metalloproteinase acting on the amyloid precursor protein (APP) as an alpha-secretase in neurons. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Relative to cybrids expressing mtDNA from CH individuals, MCI and AD cybrids contained more phosphorylated tau-217 (p-tau217), p-tau181, and total tau. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As expected, males had higher lean mass and VO2peak than females (p = 0.01), but groups did not differ in body mass index (p = 0.51). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 8,313 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.
- Brain insulin resistance in Down syndrome: Involvement of PI3K-Akt/mTOR axis in early-onset of Alzheimer's disease and its potential as a therapeutic target
- TIA1 Mutations in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia Promote Phase Separation and Alter Stress Granule Dynamics
- High-frequency oscillations arise through distinct mechanisms in models of α- synucleinopathy and channelopathy-induced epilepsy
- Extensive astrocyte infection is prominent in human immunodeficiency virus-associated dementia
- NOVEL DRUG DELIVERY SYSTEM: A PANDORA BOX FOR THE MANAGE MENT OF ALZHEIMER NOVEL DRUG DELIVERY IN ALZHEIMER
- Long-term voluntary exercise inhibited AGE/RAGE and microglial activation and reduced the loss of dendritic spines in the hippocampi of APP/PS1 transgenic mice
- Docosahexaenoic acid signalolipidomics in nutrition: significance in aging, neuroinflammation, macular degeneration, Alzheimer's, and other neurodegenerative diseases
- Protein carbonyl groups as biomarkers of oxidative stress
- Clinical and neuropathological features of the arctic APP gene mutation causing early-onset Alzheimer disease
- Genetic risk for Alzheimer's disease is concentrated in specific macrophage and microglial transcriptional networks
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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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 (3.4% 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 →