Accumulation of damaged mitochondria is a hallmark of aging and age-related neurodegeneration, including Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Accumulation of damaged mitochondria is a hallmark of aging and age-related neurodegeneration, including Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuritic plaques, a pathological hallmark in Alzheimer's disease (AD) brains, comprise extracellular aggregates of amyloid-beta (Aβ) peptide and degenerating neurites that accumulate autolysosomes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Adequate supply of blood and structural and functional integrity of blood vessels are key to normal brain functioning. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The CNS is protected by the immune system, including cells that reside directly within the CNS and help to ensure proper neural function, as well as cells that traffic into the CNS with disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-beta peptide is elevated in the brains of patients with Alzheimer disease and is believed to be causative in the disease process. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic loss is the best pathological correlate of the cognitive decline in Alzheimer's disease; however, the molecular mechanisms underlying synaptic failure are unknown. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Elevated glucocorticoid levels produce hippocampal dysfunction and correlate with individual deficits in spatial learning in aged rats. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microinfarctions are present in the aged and injured human brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Activation of innate immune receptors by host-derived factors exacerbates CNS damage, but the identity of these factors remains elusive. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We have previously shown that chronic treatment with the monoclonal antibody m266, which is specific for amyloid beta-peptide (Abeta), increases plasma concentrations of Abeta and reduces Abeta burden in the PDAPP transgenic mouse model of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A hallmark of all forms of Alzheimer's disease (AD) is an abnormal accumulation of the beta-amyloid protein (Abeta) in specific brain regions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyotrophic lateral sclerosis (ALS) is a genetically heterogeneous neurodegenerative syndrome hallmarked by adult-onset loss of motor neurons. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Experimental studies of Alzheimer's disease have largely depended on transgenic mice overexpressing amyloid precursor protein (APP). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Several pathogenic Alzheimer's disease (AD) mutations have been described, all of which cause increased amyloid beta-protein (Abeta) levels. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We investigated synaptic communication and plasticity in hippocampal slices from mice overexpressing mutated 695-amino-acid human amyloid precursor protein (APP695SWE), which show behavioral and histopathological abnormalities simulating Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a biologically complex neurodegenerative dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is associated with defects of synaptic connectivity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the single biggest unmet medical need in neurology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pericytes are vascular mural cells embedded in the basement membrane of blood microvessels. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The glucose transporter GLUT1 at the blood-brain barrier (BBB) mediates glucose transport into the brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Substantial progress has been made toward understanding the genetic architecture, cellular substrates, brain circuits and endophenotypic profiles of neuropsychiatric disorders, including autism spectrum disorders (ASD), schizophrenia and Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the most frequent neurodegenerative disorder and the most common cause of dementia in the elderly. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulation of cerebral amyloid-beta peptide (Abeta) is essential for developing synaptic and cognitive deficits in Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This widely cited review examined the long-running debate over whether amyloid or tau comes first in Alzheimer's disease. 4 key findings →
Evidence: moderate
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.
1,034 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 →