28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Transforming growth factor-beta 1 was studied as a possible regulator of messenger RNAs in astrocytes and neurons that increase after hippocampal deafferentation by perforant path transection: tubulin alpha 1, clusterin and glial fibrillary acidic protein messenger RNA. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this article the correlations between the morphological evaluation of the nerve fiber layer (NFL) thickness (by OCT) and retinal functional assessment (by Pattern ERG recordings) performed in patients affected by ocular hypertension (OHT), glaucoma (OAG), demyelinating optic neuritis (MSON), and Alzheimer's disease (AD) are reported. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
HIV-1 transactivating protein Tat is neurotoxic and is believed to play a role in the development of AIDS-associated dementia complex. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although clinical experience suggests that brain injury in the aged is associated with a poor prognosis, little research has examined this phenomenon at a cellular or molecular level. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Senile plaques (SP), a neuropathological hallmark of Alzheimer's disease (AD), are characterized by extracellular accumulations of beta amyloid (A beta). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing evidence suggests that the calcineurin (CN)-dependent transcription factor NFAT (Nuclear Factor of Activated T cells) mediates deleterious effects of astrocytes in progressive neurodegenerative conditions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glial fibrillary acidic protein (GFAP) and protein S-100B are established indicators of astrogliosis in neuropathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We describe a new human isoform, GFAP epsilon, of the intermediary filament protein GFAP (glial fibrillary acidic protein). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic neuroinflammatory processes including glial activation may play a role in the pathogenesis of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The two major intermediate filament (IF) proteins of astrocytes are vimentin and GFAP. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is characterized by the extracellular deposition of beta-amyloid peptide (Abeta) in cerebral plaques and evidence is accumulating that amyloid is neurotoxic. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the context of Alzheimer's disease (AD), hippocampal alterations have been well described in advanced stages of the pathology, when amyloid deposition, inflammation and glial activation occur, but less attention has been directed to studying early brain and behavioral changes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We have examined oxidized proteins in the brain regions of wild-type (WT) and ApoE-knockout (KO) animals. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The frequency of autoantibodies (AAbs) was surveyed in several neurodegenerative diseases, other neurological diseases, and controls using antigen-specific EIAs for neurofilament heavy subunit, tubulin, glial fibrillary acidic protein, S100 protein, tau, beta-amyloid peptide, myelin basic protein, and heparan sulfate proteoglycan. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized neuropathologically by the presence of neuritic plaques (NP) in cerebral cortex and hippocampus, as well as intraneuronal neurofibrillary tangles and granulovacuolar degeneration. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyotrophic lateral sclerosis (ALS) is a lethal neurodegenerative disease characterized by progressive muscular atrophy, paralysis and bulbar symptoms. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Abnormalities in the cerebral microvasculature are common in Alzheimer disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pre-treatment with co-ultraPEALut significantly reduced inducible nitric oxide synthase and glial fibrillary acidic protein expression, restored neuronal nitric oxide synthase and brainderived neurotrophic factor and reduced the apoptosis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Fluoro-Jade B is known as a high affinity fluorescent marker for the localization of neuronal degeneration during acute neuronal distress. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Somatostatin, widely distributed in human cortical brain regions, acts through specific high affinity somatostatin receptors (SSTR1-5) to exert profound effects on motor, sensory, behavioral, cognitive and autonomic functions. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitive decline in Alzheimer's disease (AD) occurs as a result of the buildup of pathological proteins and downstream events including an elevated and altered inflammatory response. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In mammalian central nervous system, neurogenesis occurs in the hippocampus and the subventricular zone (SVZ). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glycosylation influences the biological activity of proteins and affects their folding and stability. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
It is well-established that glial cells play an important role during injury and neurodegenerative processes in the central nervous system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
It has been hypothesized that increased expression of proinflammatory cytokines mediate a variety of central nervous system disorders such as multiple sclerosis, Alzheimer's disease, cerebral ischemia, spinal cord injury, HIV encephalopathy and chronic pain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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.
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 28,180 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 (3.7% 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 →