Alzheimer's disease (AD) is the most common cause of dementia worldwide. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neuroblastoma cell lines such as SH-SY5Y are the most frequently utilized models in neurodegenerative research, and their use has advanced the understanding of the pathology of neurodegeneration over the past few decades. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The aberrant metabolism of amyloid-β protein (Aβ) in the human brain has been implicated in the etiology of Alzheimer disease (AD). γ-Secretase is the enzyme that generates various forms of Aβ, such as Aβ40 and Aβ42, the latter being an aggregation-prone toxic peptide that is involved in the pathogenesis of AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
S100B is typically elevated in AD cases; however, the increased levels in African Americans here may be indicative of increased severity in specific populations. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common neurodegenerative disorder without effective treatment so far. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is associated to depressed brain energy supply and impaired cortical and hippocampal synaptic function. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
The search for a blood-based biomarker that identifies Alzheimer's disease (AD) and can replace current invasive and expensive diagnostic tests, continues. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Here, we found that overexpression of human wild-type full-length MAPT, which models MAPT pathologies as seen in sporadic AD patients, induced autophagy deficits via repression of autophagosome-lysosome fusion leading to significantly increased LC3 (microtubule-associated protein 1 light chain 3)-II and SQSTM1/p62 (sequestosome 1) protein levels with autophagosome accumulation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dysfunction of cell bioenergetics is a common feature of neurodegenerative diseases, the most common of which is Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (apoE) is a lipid carrier in both the peripheral and the central nervous systems. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Gene and protein expression data provide useful resources for understanding brain function, but little is known about the lipid composition of the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
Diabetes and impaired brain insulin signaling are linked to the pathogenesis of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
None of the proposed mechanisms of Alzheimer's disease (AD) fully explains the distribution patterns of the neuropathological changes at the cellular and regional levels, and their clinical correlates. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Human age-associated traits, such as cognitive decline, can be highly variable across the population, with some individuals exhibiting traits that are not expected at a given chronological age. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The existing large-scale genome-wide association studies (GWAS) datasets provide strong support for investigating the mechanisms of Alzheimer's disease (AD) by applying multiple methods of pathway analysis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the classical hallmarks of Aβ-deposition and tau-pathology that are thought to ultimately lead to synapse and neuron loss. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies have demonstrated the importance of microglia in AD pathogenesis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
Clusterin, also known as apoJ, is a lipoprotein abundantly expressed within the CNS. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glycoprotein non-metastatic melanoma protein B (GPNMB) is a type I transmembrane glycoprotein first identified in low-metastatic human melanoma cell lines as a regulator of tumor growth. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglial cell function is implicated in the etiology of Alzheimer's disease by human genetics. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The downregulation of TREM2 exacerbated surgery-induced cognitive deficits and exaggerated neuroinflammatory responses in this rodent model. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
Heterozygous triggering receptor expressed on myeloid cells (TREM2) mutations are an Alzheimer's disease (AD) risk factor. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutation of Triggering receptor expressed on myeloid cells 2 (TREM2) impairs the response of microglia to amyloid-β (Aβ) pathology in Alzheimer's disease (AD), although the mechanism governing TREM2-regulated microglia recruitment to Aβ plaques remains unresolved. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease, characterized by neuroinflammation and beta-amyloid protein plaques, is a memory-threatening neurodegenerative disease with no effective treatment. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurons and microglia are two major components in the central nervous system (CNS). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 7,975 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.
- Predicting the Beneficial Effects of Cognitive Stimulation and Transcranial Direct Current Stimulation in Amnestic Mild Cognitive Impairment with Clinical, Inflammation, and Human Microglia Exposed to Serum as Potential Markers: A Double-Blind Placebo-Controlled Randomized Clinical Trial
- Astrocytic APOE4 removal confers cerebrovascular protection despite increased cerebral amyloid angiopathy
- Role of the low-density lipoprotein receptor-related protein in beta-amyloid metabolism and Alzheimer disease
- Reduced hippocampal insulin-degrading enzyme in late-onset Alzheimer's disease is associated with the apolipoprotein E-epsilon4 allele
- Midlife systemic inflammatory markers are associated with late-life brain volume: The ARIC study
- Down syndrome: age-dependence of PiB binding in postmortem frontal cortex across the lifespan
- Glial-neuronal interactions in Alzheimer's disease: the potential role of a 'cytokine cycle' in disease progression
- Contributions of Cerebro-Cerebellar Default Mode Connectivity Patterns to Memory Performance in Mild Cognitive Impairment
- Regional tau pathology and loneliness in cognitively normal older adults
- Neuropathological stageing of Alzheimer-related changes
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 29,380 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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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 →