Tau interacts with α-Synuclein (α-Syn) and co-localizes with it in the Lewy bodies, influencing α-Syn pathology in Parkinson's disease (PD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Distinct neuronal and glial tau pathologies define corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP). 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cortical synaptic loss has emerged as an early abnormality in Alzheimer's disease (AD) with a strong relationship to cognitive performance. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Protein aggregation caused by the disruption of proteostasis will lead to cellular cytotoxicity and even cell death, which is implicated in multiple neurodegenerative diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our understanding of stress granule (SG) biology has deepened considerably in recent years, and with this, increased understanding of links has been made between SGs and numerous neurodegenerative diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Protein misfolding is a fundamental biological process with profound implications for human health and disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Fifteen cases were identified (14 men). All had clear histories of dream enactment behavior, and 10 had RBD confirmed by polysomnography. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical and neuropathologic data in 45 patients with Parkinson's disease (PD) were compared. 3 key findings →
Participants: 45 Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
A major barrier to research on Parkinson's disease is inaccessibility of diseased tissue for study. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD) and prion diseases, deposits of aggregated disease-specific proteins are found. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular dementia (VD) is the second most common dementia syndrome worldwide, and effective treatments are lacking. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings highlight the potential of serum NfL as a useful surrogate end point of disease severity in upcoming targeted treatments. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
We present a 86-year-old woman without relevant medical history and two brothers who died by dementia, who started at 55 years with depression and personality changes with ongoing worsening (>30 years) and functional decline. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The aim of the present study was to investigate, in patients with Alzheimer's disease (AD), and vascular dementia (VAD), patterns of local release of vascular endothelial growth factor (VEGF) and transforming growth factor-beta (TGF-beta), two cytokines having a pivotal role in hypoxia-induced angiogenesis. 3 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
The idea that eye movements can reflect certain aspects of brain function and inform on the presence of neurodegeneration is not a new one. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The VRFCAT-SL appears to provide a useful measure of cognitive functional capacity that is not confounded by PD motor symptoms. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pathological hallmarks of Parkinson's disease (PD) are the progressive loss of dopaminergic neurons in the substantia nigra and the formation of Lewy bodies (LBs) in remaining neurons. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings provide novel insights into the genetic determinants of LBD and the shared genetic etiology and biological mechanisms of LBD, AD, and PD, which could benefit the understanding of the co-pathology as well as the potential treatment of these diseases simultaneously. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Calcium dysregulation ("Calcium Hypothesis") is an early and critical event in Alzheimer's and other neurodegenerative diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
DNA methylation is critical for the normal development and functioning of the human brain, such as the proliferation and differentiation of neural stem cells, synaptic plasticity, neuronal reparation, learning, and memory. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the presence of β-amyloid (Aβ) and tau, and subcortical vascular cognitive impairment (SVCI) is characterized by cerebral small vessel disease (CSVD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia with Lewy bodies (DLB) is the second most common cause of neurodegenerative dementia after Alzheimer's disease (AD). 1 key finding →
Participants: 21 Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Although motor impairments in Parkinson's disease (PD) are attributed to nigrostriatal dopaminergic denervation, postural instability and gait difficulty (PIGD) features are less responsive to dopaminergic medications. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
The major genetic cause of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) is a C9orf72 G 4 C 2 repeat expansion 1,2 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
The PERK-eIF2α branch of the Unfolded Protein Response (UPR) mediates the transient shutdown of translation in response to rising levels of misfolded proteins in the endoplasmic reticulum. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 2,748 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.
- Cerebrospinal fluid biomarkers in Alzheimer's disease, vascular dementia and ischemic stroke patients: a critical analysis
- Huntington's disease: present treatments and future therapeutic modalities
- NRF2 and NF-қB interplay in cerebrovascular and neurodegenerative disorders: Molecular mechanisms and possible therapeutic approaches
- Altered spatiotemporal brain dynamics of interoception in behavioural-variant frontotemporal dementia
- Meta-analysis of glucose metabolism across Alzheimer's, Parkinson's and ALS reveals distinct patterns of cortical hypometabolism versus subcortical hypermetabolism with disease-specific spatial signatures
- Refining the diagnostic accuracy of Parkinsonian disorders using metaphenomic annotation of the clinicopathological literature
- A pathogenic Tau mutation drives autophagy-lysosome dysfunction that limits Tau degradation in a model of frontotemporal dementia
- Apolipoprotein E Gene in α-Synucleinopathies: A Narrative Review
- Neuropsychiatric symptoms profile and markers of Alzheimer disease-type pathology in patients with Lewy body dementias
- The A53T alpha-synuclein mutation increases iron-dependent aggregation and toxicity
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 30,180 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.
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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →