The innate immune system plays an integral role in the progression of many neurodegenerative diseases. 4 key findings →
Participants: 148 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.
Beta-amyloid deposition is a defining feature of Alzheimer's disease (AD). 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The analytic sample included 469 participants (mean age 71.2 ± 8.5 years, 53% female). 3 key findings →
Design: cohort Participants: 469 Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
Previously derived polygenic risk scores (PRSs) for Alzheimer's disease (AD) perform inconsistently across diverse ancestries. 3 key findings →
Design: cohort Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E (Apo-E) is a major cholesterol carrier that supports lipid transport and injury repair in the brain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The combined measure of CSF Abeta42 and tau meets the requirements for clinical use in discriminating AD from normal aging and specific neurologic disorders. 4 key findings →
Participants: 84 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
56/100
Our findings suggest that inflammation in the CNS increases in normal aging and is intimately related to markers of neurodegeneration in the preclinical stages of AD and SNAP. sAPPβ and β-secretase activity are not useful diagnostic or staging markers in preclinical AD. 2 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
56/100
Individuals with neuropsychiatric, cardiovascular, and sensory impairment/cancer patterns are at increased risk for dementia and APOE ε4, and inflammation may further increase the risk. 3 key findings →
Participants: 2,478 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is a progressive neurodegenerative disease most often associated with memory deficits and cognitive decline, although less common clinical presentations are increasingly recognized. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We detected large numbers of HLA-DR-positive reactive microglia (macrophages), along with Lewy bodies and free melanin, in the substantia nigra of all cases studied with Parkinson's disease (5) and parkinsonism with dementia (PD) (5). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease is the most common cause of dementia worldwide, with the prevalence continuing to grow in part because of the aging world population. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CLBs detected by alpha-synuclein antibodies in patients with PD are a more sensitive and specific correlate of dementia than the presence of Alzheimer's pathology, which was present in a minority of the cases in this series. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Early reports of cognitive and behavioural deficits in motor neuron disease might have been overlooked initially, but the concept of a frontotemporal dementia-motor neuron disease continuum has emerged during the past decade. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The blood-brain barrier (BBB) is a continuous endothelial membrane within brain microvessels that has sealed cell-to-cell contacts and is sheathed by mural vascular cells and perivascular astrocyte end-feet. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Postmortem MRI scans were obtained for the first 56 participants of the Nun Study who were scanned. 1 key finding →
Participants: 56 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Systemic inflammation is associated with ischemia and Alzheimer disease (AD). 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
MRI volumes measured over time are valid biomarkers of pathologic progression of AD across a range of antemortem clinical states. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The INNOTEST and INNO-BIA CSF platforms perform equally well in identifying individuals with underlying amyloid plaque pathology. 2 key findings →
Participants: 103 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In vivo imaging and quantification of amyloid-β plaque (Aβ) burden in small-animal models of Alzheimer's disease (AD) is a valuable tool for translational research such as developing specific imaging markers and monitoring new therapy approaches. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
MRI studies have provided valuable insights into the structure and function of neural networks, particularly in health and in classical neurodegenerative conditions such as Alzheimer disease. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
56/100
DCTclock discriminates between diagnostic groups and improves upon traditional cognitive tests for detecting biomarkers of amyloid and tau pathology in CN older adults. 3 key findings →
Participants: 300 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
56/100
The results suggest that difficulty in identifying familiar odours in old age is partly due to the accumulation of neurofibrillar pathology in central olfactory regions. 2 key findings →
Participants: 166 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A hexanucleotide-repeat expansion in C9ORF72 is the most common genetic variant that contributes to amyotrophic lateral sclerosis and frontotemporal dementia 1,2 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Physical frailty in old age is associated with Alzheimer disease pathology in older persons with and without dementia. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Age-related increases in dementia risk can be attributed to accumulation of multiple pathologies, each of which contributes to dementia risk. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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.
- Role of the toll-like receptor 4 in neuroinflammation in Alzheimer's disease
- Human TDP-43 expression worsens FTD-related phenotypes in progranulin-insufficient mice
- Age-Related Cognitive Decline and Dementia: Interface of Microbiome–Immune–Neuronal Interactions
- Phosphorylated tau interactome in the human Alzheimer's disease brain
- Monoamine Oxidase‐B (MAO‐B) Identifies Neurotoxic Reactive Astrocytes in Alzheimer's Disease and Related Dementias
- Prion-like properties of pathological TDP-43 aggregates from diseased brains
- The neuroprotection of liraglutide on Alzheimer-like learning and memory impairment by modulating the hyperphosphorylation of tau and neurofilament proteins and insulin signaling pathways in mice
- Overexpression of human S100B exacerbates cerebral amyloidosis and gliosis in the Tg2576 mouse model of Alzheimer's disease
- TREM2 Deficiency Aggravates NLRP3 Inflammasome Activation and Pyroptosis in MPTP-Induced Parkinson's Disease Mice and LPS-Induced BV2 Cells
- Environmental enrichment mitigates cognitive deficits in a mouse model of Alzheimer's disease
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 →