The hippocampus is one of the most well studied structures in the human brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Postmortem demonstration of increased expression of biologically active S100B in Alzheimer's disease (AD) and its relation to progression of neuropathological changes across the cortical regions suggests involvement of this astrocytic cytokine in the pathophysiology of AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease (AD) is the most common neurodegenerative disorder that affects the elderly. 4 key findings →
Evidence: low
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Huntington's disease (HD) is a fatal inherited neurodegenerative disorder characterized by personality changes, motor impairment, and subcortical dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Sporadic, late-onset Alzheimer disease (AD) constitutes the most frequent cause of dementia in the elderly population. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a late-onset dementia that is characterized by the loss of memory and an impairment of multiple cognitive functions. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebrovascular dysfunction contributes to the cognitive decline and dementia in Alzheimer's disease (AD), and may precede cerebral amyloid angiopathy and brain accumulation of the Alzheimer's neurotoxin, amyloid beta-peptide (Abeta). 4 key findings →
Evidence: low
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Neuropathologic examination of 3 patients with Alzheimer disease in the Elan Pharmaceuticals trial using antibodies specific for different Abeta species showed in one case, 4 months after the immunization, evidence of a stage of active plaque clearance with "moth-eaten" plaques and abundant Abeta phagocytosis by microglia. 4 key findings →
Evidence: low
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Stress granules (SGs) are RNA-containing cytoplasmic foci formed in response to stress exposure. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Gangliosides are the main glycolipids of neuronal plasma membranes. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
45/100
TDP-43 is an RNA/DNA-binding protein implicated in transcriptional repression and mRNA processing. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia are a major ghal component of the central nervous system (CNS) and are extremely sessile. 4 key findings →
Evidence: low
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Alzheimer Disease (AD) is a neurodegenerative disorder and the most common form of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The colony-stimulating factor-1 receptor (CSF-1R) kinase regulates tissue macrophage homeostasis, osteoclastogenesis, and Paneth cell development. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent findings suggest that hypercholesterolemia may contribute to the onset of Alzheimer's disease-like dementia but the underlying mechanisms remain unknown. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia constitute the primary resident immune surveillance cell in the brain and are thought to play a significant role in the pathogenesis of several neurodegenerative disorders, such as Alzheimer's disease, multiple sclerosis, Parkinson's disease and HIV-associated dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Enriched populations of human microglial cells were isolated from mixed cell cultures prepared from embryonic human telencephalon tissues. 4 key findings →
Evidence: low
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The decline in mental fitness associated with Alzheimer disease is accompanied by physical changes in the brain, including the development of characteristic plaques and neurofibrillary tangles, but the pathogenesis of those changes is not clear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We presently describe the full-length cloning and functional characterization of an HIV-1-inducible gene, astrocyte elevated gene (AEG)-1. 4 key findings →
Evidence: low
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The expression of the purinergic receptor subtype P2X(7)R, a nonselective cationic channel activated by high levels of adenosine triphosphate (ATP), has been studied in adult microglia obtained from Alzheimer disease (AD) and nondemented (ND) brains, in fetal human microglia exposed to Abeta(1-42) peptide and in vivo in Abeta(1-42)-injected rat hippocampus. 4 key findings →
Evidence: low
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Amyloid-β plaques and neurofibrillary tangles are the main neuropathological hallmarks in Alzheimer's disease (AD), the most common cause of dementia in the elderly. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Kir4.1 is an inwardly rectifying K(+) channel expressed exclusively in glial cells in the central nervous system. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis with D,L-buthionine-S,R-sulfoximine (BSO) causes human microglia, human astrocytes, THP-1 cells, and U373 cells to secrete materials toxic to human neuroblastoma SH-SY5Y cells and stimulates them to release TNF-alpha, IL-6, and nitrite ions. 4 key findings →
Evidence: low
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Astrocytes are glial cells that are distributed throughout the central nervous system in an arrangement optimal for chemical and physical interaction with neuronal synapses and brain blood supply vessels. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease (AD) is the most common cause of dementia in the elderly, and the fourth leading cause of death in the United States. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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.
- TREM2 regulates microglial cell activation in response to demyelination in vivo
- Receptors make the pathway choice for protein degradation
- Immunoreactivity of presenilin-1 in human, rat and mouse brain
- The role of microbial amyloid in neurodegeneration
- The case for rejecting the amyloid cascade hypothesis
- Caspase dependent DNA fragmentation might be associated with excitotoxicity in Alzheimer disease
- The DYRK1A gene, encoded in chromosome 21 Down syndrome critical region, bridges between beta-amyloid production and tau phosphorylation in Alzheimer disease
- Roles of amyloid precursor protein and its fragments in regulating neural activity, plasticity and memory
- Amyloid-beta aggregation implicates multiple pathways in Alzheimer's disease: Understanding the mechanisms
- The effects of chronic glucocorticoid exposure on dendritic length, synapse numbers and glial volume in animal models: implications for hippocampal volume reductions in depression
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 →