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
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
39/100
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive memory loss due to aberrant accumulation of misfolded proteins inside and outside neurons and glial cells, leading to a loss of cellular protein homeostasis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Protein homeostasis, or proteostasis, has an important regulatory role in cellular function. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathy is one of the pathological features of Alzheimer's disease and related dementias (ADRD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Retrograde bias better predicted tau progression than anterograde bias, but our best-fitting biophysical models incorporate the mixed effects of both retrograde- and anterograde-directed spread, with notable tau-strain-specific differences. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Transgenic iPSC lines provide a unique tool to study the molecular and genetic mechanisms of FTDP-17 caused by the presence of the c.2013T > G (p.N279K) mutation, as well as to test potential drugs in vitro. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer’s disease (AD) is the most prevalent cause of dementia, characterized by progressive cognitive decline, amyloid-β (Aβ) plaques, and neurofibrillary tangles composed of hyperphosphorylated tau protein. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
38/100
Alcohol use disorder (AUD) is linked with changes in brain structure and function, with robust evidence for neurodegenerative changes, including synaptic loss in preclinical models. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
38/100
Primary and secondary tauopathies are major causes of dementia characterized by the abnormal accumulation of microtubule-associated protein tau. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Patients with Alzheimer's disease (AD) have two types of abnormal protein buildups: amyloid plaques and neurofibrillary tangles, in addition to the early synaptic dysfunction associated with the enzymes acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Fifteen cases were identified, spanning argyrophilic grain disease, primary age-related tauopathy, corticobasal degeneration, genetic frontotemporal dementia, and progressive supranuclear palsy. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
High Resolution Image Download MS PowerPoint Slide Abnormal accumulation of tau fibrillar aggregates is a hallmark of tauopathies, including Alzheimer’s disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tau protein plays a pivotal role in maintaining neuronal structure and function through its regulation of microtubule stability and neuronal polarity. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neurodegenerative diseases are currently among the most devastating diseases with no effective disease-modifying drugs in the market, with Alzheimer's disease (AD) being the most prevalent. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
38/100
The study of Alzheimer's disease (AD)-associated mutations has implicated dysregulation of amyloid precursor protein (APP) proteolysis in the disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), the most prevalent form of dementia, is characterized by hallmark pathologies such as amyloid-beta (Aβ) plaque accumulation, tau hyperphosphorylation, and progressive neuronal dysfunction. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tau hyperphosphorylation has been considered a major contributor to neurodegeneration in Alzheimer's disease (AD) and frontotemporal dementia, and related tauopathies have gained prominence in the development of therapies for these conditions. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the leading cause of dementia worldwide and represents a growing public health challenge in aging societies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most common form of dementia worldwide. β-amyloid peptide (Aβ) is currently assumed to be the main cause of synaptic dysfunction and cognitive impairments in AD, but the molecular signaling pathways underlying its neurotoxic consequences have not yet been completely explored. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
It is increasingly accepted that early cognitive impairment in Alzheimer's disease results in considerable part from synaptic dysfunction caused by the accumulation of a range of oligomeric assemblies of amyloid β-protein (Aβ). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aggregates of the microtubule-associated protein tau are a defining feature of several neurodegenerative diseases that are collectively known as tauopathies, and constitute one of the hallmark lesions of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a prevalently found tauopathy characterized by memory loss and cognitive insufficiency. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We will consider also emerging data dealing with potential therapeutic approaches for ameliorating the cognitive and memory deficits associated with these disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by an asymptomatic period of amyloid-β (Aβ) deposition as insoluble extracellular plaque, intracellular tau aggregation, neuronal and synaptic loss, and subsequent cognitive dysfunction and dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 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.
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 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 →