The amyloid-β oligomer (AβO) hypothesis was introduced in 1998. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The amyloid-β oligomer (AβO) hypothesis was introduced in 1998. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Both Alzheimer's disease and senile dementia of the Alzheimer type (AD/SDAT) are progressive dementias characterized neuropathologically by the presence in the cerebral cortex of numerous neurofibrillary tangles and neuritic plaques. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases share the fact that they derive from altered proteins that undergo an unfolding process followed by formation of β-structures and a pathological tendency to self-aggregate in neuronal cells. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The ageing of the human brain is a cause of cognitive decline in the elderly and the major risk factor for Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a devastating neurodegenerative disorder without a cure. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cholinergic synapses are ubiquitous in the human central nervous system. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondria continuously undergo two opposing processes, fission and fusion. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Profound neuronal dysfunction in the entorhinal cortex contributes to early loss of short-term memory in Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cyclophilin D (CypD, encoded by Ppif) is an integral part of the mitochondrial permeability transition pore, whose opening leads to cell death. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Insulin is a peptide secreted by the pancreas and plays an important role in the regulation of glucose metabolism in peripheral tissues. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chemical synapses are the predominant neuron-to-neuron contact in the central nervous system. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Brain cholinergic neurons are critical for memory function and their loss may contribute to memory impairment in Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Identifying reliable biomarkers of aging is a major goal in geroscience. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Most proteins must fold into defined three-dimensional structures to gain functional activity. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Autophagy is a lysosomal degradative process used to recycle obsolete cellular constituents and eliminate damaged organelles and protein aggregates. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Oxidative stress is known to play an important role in the pathogenesis of a number of diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Oxidative stress is proposed as a regulatory element in ageing and various neurological disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is one of the most prevalent neurodegenerative diseases, characterized by impaired cognitive function due to progressive loss of neurons in the brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Stress proteins located in the cytosol or endoplasmic reticulum (ER) maintain cell homeostasis and afford tolerance to severe insults. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Decades of research indicate mitochondria from Alzheimer's disease (AD) patients differ from those of non-AD individuals. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A variable combination of developmental delay, retinitis pigmentosa, dementia, seizures, ataxia, proximal neurogenic muscle weakness, and sensory neuropathy occurred in four members of a family and was maternally transmitted. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ensuring cellular protein homeostasis, or proteostasis, requires precise control of protein synthesis, folding, conformational maintenance, and degradation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is conceptualized as a progressive consequence of two hallmark pathological changes in grey matter: extracellular amyloid plaques and neurofibrillary tangles. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing numbers of individuals, particularly the elderly, suffer from neurodegenerative disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mean scores of emotional distress were significantly higher in carers at each time point than in controls (all p<0.0003). 2 key findings →
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 →