27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
To demonstrate this hypothesis, we established abnormalities in the glucose metabolism utilizing thiamine deficiency in vitro and in vivo, and we found dramatically reduced dendrite spine density. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dozens of genes have been implicated in late onset Alzheimer's disease (AD) risk, but none has a defined mechanism of action in neurons. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genetically modified mice have provided insights into the progression and pathology of Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is emerging as a synaptopathology driven by metaplasticity. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The term proteostasis reflects the fine-tuned balance of cellular protein levels, mediated through a vast network of biochemical pathways. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Protein homeostasis (proteostasis) refers to the ability of cells to preserve the correct balance between protein synthesis, folding and degradation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The ubiquitin-proteasomal-system (UPS) and the autophagy-lysosomal-system (ALS) are both highly susceptible for disturbances leading to the accumulation of cellular damage. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Imbalance of neuronal proteostasis associated with misfolding and aggregation of Tau protein is a common neurodegenerative feature in Alzheimer's disease (AD) and other Tauopathies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neutral sphingomyelinase smpd3 is most abundantly expressed in neurons of brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuronal signaling depends on the exocytic fusion and subsequent endocytic retrieval and reformation of neurotransmitter-containing synaptic vesicles at synapses. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In normal physiological condition, the maintenance of cellular proteostasis is a prerequisite for cell growth, functioning, adapting to changing micro-environments, and responding to extracellular stress. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Age is the common risk factor for both neurodegenerative and neuromuscular diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Insulin resistance (IR), a key component of the metabolic syndrome, precedes the development of diabetes, cardiovascular disease, and Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Over the past two decades, caregiver stress has been the subject of scientific inquiry by investigators around the world representing a variety of disciplines. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Perceived burden was directly and significantly related to depression for both spouse caregivers and adult child caregivers. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
AimTo explore the experiences and challenges for residential care home staff when managing the healthcare needs of their residents, in particular those living with dementia. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Improved and earlier advanced care planning for persons with dementia and their caregivers can help delineate goals of care and prepare for the inevitable complications of end-stage dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disease that develops insidiously and causes dementia finally. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Traumatic brain injury (TBI) is a major health and economic burden. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Medicare costs were reduced from hospice election until death using both 2009-2010 and new 2016 payment structures and rates. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Diabetes care guidelines recommend more relaxed glycemic targets for patients with specific chronic conditions because they are thought to have an increased risk of hypoglycemia, limited life expectancy, and/or high clinical complexity. 3 key findings →
Participants: 216,839 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
AAV-mediated progranulin delivery reduced lipofuscinosis in Grn -/- mice even after the onset of pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Emerging evidence indicates that moderate intensity aerobic exercise is positively correlated with cognitive function and memory. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Moreover, they exhibit decreased astrocyte and microglial activation markers GFAP and CD68, suggesting that a suppressed neuroinflammatory response may be implicated in human brain resilience to Alzheimer's pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aggregation of tau into fibrillar structures within the CNS is a pathological hallmark of a clinically heterogeneous set of neurodegenerative diseases termed tauopathies. 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 27,380 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →