27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Insurmountable evidence has demonstrated a strong association between Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA), along with various other cerebrovascular diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
While prevailing evidence supports that the amyloid cascade hypothesis is a key component of Alzheimer's disease (AD) pathology, many recent studies indicate that the vascular system is also a major contributor to disease progression. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Perlecan is a heparan sulfate proteoglycan protein in the extracellular matrix that structurally and biochemically supports the cerebrovasculature by dynamically responding to changes in cerebral blood flow. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Androgens affect the cerebral vasculature and may contribute to sex differences in cerebrovascular diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Through a number of an extensive autopsy, biomarker, and genomics studies, researchers have recently defined a novel type of dementia known as limbic-predominant age-related TDP-43 encephalopathy (LATE). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recently, a consensus working group provided new terminology for a common disease entity, limbic predominant age-related TDP-43 encephalopathy (LATE), and its neuropathological substrate (LATE-NC). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
It is important to have a wide perspective to provide appropriate medical care for the oldest-old individuals. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
TAR DNA binding protein (TDP-43) is a DNA/RNA binding protein whose pathological role in amyotrophic lateral sclerosis (ALS) and frontal temporal lobe dementia (FTLD) via formation of protein aggregates is well established. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This review considers whether the Braak hypothesis on protein propagation could account for prion disease, particularly Creutzfeldt-Jakob disease (CJD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Since the discovery of TAR DNA-binding protein 43 (TDP-43) in 1995, our understanding of its role continues to expand as research progresses. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mus treatment attenuated memory dysfunction, reduced Aβ level, and enhanced synaptic plasticity in APP/PS1 mice. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hippocampal synaptic dysfunction is a hallmark of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The strength and efficiency of synaptic connections are affected by the environment or the experience of the individual. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dendrites and dendritic spines are dynamic structures with pivotal roles in brain connectivity and have been recognized as the locus of long-term synaptic plasticity related to cognitive processes such as learning and memory. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic plasticity is the neural basis of physiological processes involved in learning and memory. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disease characterized by neurological dysfunction, including memory impairment, attributed to the accumulation of amyloid β (Aβ) in the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Actin-depolymerization factor (ADF)/cofilin, a family of actin-binding proteins, are critical for the regulation of actin reorganization in response to various signals. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found a beginning synaptic impairment (LTP deficit) at 3-4 months in the prefrontal cortex of AppNL-G-F mice that is further aggravated and extended to the hippocampus at 6-8 months. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic dysfunction has been implicated as an early cause of cognitive decline in neurodegenerative diseases (NDDs) such as Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by Aβ-driven synaptic dysfunction in the early phases of pathogenesis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia, most prevalent in the elderly population and has a significant impact on individuals and their family as well as the health care system and the economy. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Intracellular accumulation of amyloid-β protein (Aβ) is an early event in Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sex differences in diseases involving oxidative and proteolytic stress are common, including greater ischemic heart disease, Parkinson disease and stroke in men, and greater Alzheimer disease in women. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Stress granules (SGs) are membraneless organelles formed in response to insult. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Protein homeostasis or proteostasis is an essential balance of cellular protein levels mediated through an extensive network of biochemical pathways that regulate different steps of the protein quality control, from the synthesis to the degradation. 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 →