Abeta protofibrils are likely to be intermediates in the in vitro assembly of Abeta amyloid fibrils, but their in vivo role has yet to be determined. 1 key finding →
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.
Although amyloid-beta peptide (Abeta) is the neurotoxic species implicated in the pathogenesis of Alzheimer's disease (AD), mechanisms through which intracellular Abeta impairs cellular properties, resulting in neuronal dysfunction, remain to be clarified. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
The cDNAs of two new human membrane-associated aspartic proteases, memapsin 1 and memapsin 2, have been cloned and sequenced. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic dysfunction and the loss of synapses are early pathological features of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Oligomeric forms of amyloid-β peptide (Aβ) are thought to play a pivotal role in the pathogenesis of Alzheimer's disease (AD), but the mechanism involved is still unclear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Inflammation is a critical component of the pathogenesis of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder for which numerous mouse models have been generated. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In light of the rising prevalence of Alzheimer's disease (AD), new strategies to prevent, halt, and reverse this condition are needed urgently. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder for which there are few therapeutics that affect the underlying disease mechanism. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondria form a highly interconnected tubular network throughout the cell via a dynamic process, with mitochondrial segments fusing and breaking apart continuously. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD), the most common neurodegenerative disorder, is a growing public health problem and still lacks effective treatments. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The beta-amyloid precursor protein (beta APP) is a membrane-spanning glycoprotein that is the source of the beta-amyloid peptide (beta AP) which accumulates as senile plaques in the brains of patients with Alzheimer's disease. beta APP is normally processed such that a cleavage occurs within the beta AP, liberating secreted forms of beta APP (APPss) from the cell. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
sorLA (Sorting protein-related receptor) is a type-1 membrane protein of unknown function that is expressed in neurons. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
In several pedigrees of early onset familial Alzheimer's disease (FAD), point mutations in the beta-amyloid precursor protein (APP) gene are genetically linked to the disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by amyloid-beta (Abeta)-containing plaques, neurofibrillary tangles, and neuron and synapse loss. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is associated with regional reductions in fluorodeoxyglucose positron emission tomography (FDG PET) measurements of the cerebral metabolic rate for glucose, which may begin long before the onset of histopathological or clinical features, especially in carriers of a common AD susceptibility gene. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Oxidative stress has been implicated to play a crucial role in the pathogenesis of a number of diseases, including neurodegenerative disorders, cancer, and ischemia, just to name a few. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The senescence-accelerated mouse (SAM) is an accelerated aging model that was established through phenotypic selection from a common genetic pool of AKR/J strain of mice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the presence of neurofibrillary tangles, senile plaques and loss of synapses. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease, an age-related neurodegenerative disorder, is characterized clinically by a progressive loss of memory and cognitive functions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The concept of molecular mimicry was established to explain commonalities of structure which developed in response to evolutionary pressures. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
DNA methylation is a major epigenetic modification that regulates gene expression. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A PET tracer is desired to help guide the discovery and development of disease-modifying therapeutics for neurodegenerative diseases characterized by neurofibrillary tangles (NFTs), the predominant tau pathology in Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurofibrillary tangles (NFTs) made up of aggregated tau protein have been identified as the pathologic hallmark of several neurodegenerative diseases including Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Gray matter atrophy, glucose hypometabolism, and β-amyloid Aβ deposition are well-described hallmarks of Alzheimer's disease, but their relationships are poorly understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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.
- Microglial senescence contributes to female-biased neuroinflammation in the aging mouse hippocampus: implications for Alzheimer's disease
- Disease-Associated Microglia: A Universal Immune Sensor of Neurodegeneration
- Astrocytes in Alzheimer's Disease: Pathological Significance and Molecular Pathways
- Genome‐wide association analysis identifies APOE as a mitophagy modifier in Lewy body disease
- Role of apolipoprotein E in neurodegenerative diseases
- Neuronal death induced by nanomolar amyloid β is mediated by primary phagocytosis of neurons by microglia
- Neuropathologically mixed Alzheimer's and Lewy body disease: burden of pathological protein aggregates differs between clinical phenotypes
- The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid beta accumulation in mice
- Review: modulating factors in amyloid-beta fibril formation
- Reduction in neurons immunoreactive for calcium-binding proteins in the anteroventral thalamic nuclei of individuals with Down syndrome
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 →