Phenoconverters had higher FW in the NBM and posterior SN. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Phenoconverters had higher FW in the NBM and posterior SN. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BackgroundSleep disturbances often precede motor symptoms in neurodegenerative diseases like Parkinson's disease (PD) and dementia with Lewy bodies (DLB). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Median survival from symptom onset was longest in SD (11.9 years) and shortest in LPA (7 years). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Chronic cerebral hypoperfusion can lead to neuronal necrosis, trigger inflammatory responses, promote white matter damage, and ultimately result in cognitive impairment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Accurate diagnosis of frontotemporal dementia (FTD) with right anterior temporal lobe (RATL) predominance remains challenging due to lack of clinical characterization, and standardized terminology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Small extracellular vesicles (sEVs), including exosomes as a subtype, with a diameter typically less than 200 nm and originating from the endosomal system, are capable of transporting a diverse array of bioactive molecules, including proteins, nucleic acids, and lipids, thereby facilitating intercellular communication and modulating cellular functions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Loss-of-function mutations affecting the lysosomal protein progranulin are a leading cause of frontotemporal dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The thematic analysis identified 12 themes: manifestations, sexual practices, impact, control, emotional formulations, beliefs in causes of hypersexuality and attributions, relationship with the partner, dealing with hypersexuality, coping with hypersexuality, self-image, stigma and professional help-seeking. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The drive for positive social interactions, or "social rewards", is an important motivator of human behaviour, conferring several adaptive benefits. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Nucleocytoplasmic transport defects are observed in Alzheimer's disease (AD) and frontotemporal dementia (FTD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Both LBDs and SPs exhibit distinct visual aberrations, ranging from minor metamorphopsias to complex hallucinations. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A network neuroscience perspective can significantly advance the understanding of neurodegenerative disorders, particularly frontotemporal dementia (FTD). 5 key findings →
Participants: 28 Evidence: moderate
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We dissociated four key cognitive components underlying remote thinking: spontaneous associative thinking, inhibition of unoriginal responses, intentional remote associative thinking, and verbal initiation; and replicated them in three independent datasets. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Emerging evidence implicating glymphatic dysfunction contributes to the pathogenesis of frontotemporal dementia (FTD). 3 key findings →
Participants: 37 Evidence: low
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Two distinct subtypes emerged. Subtype 1 (n = 63) features localized supra-normal gray matter volume deviations in dorsolateral prefrontal regions, elevated free water indicating microstructural disruption, executive dysfunction, and transcriptional enrichment in metabolic dysfunction and neurodegenerative pathways. 5 key findings →
Participants: 115 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Traumatic brain injury (TBI) has been linked to the development of neurodegenerative diseases, particularly Alzheimer's disease (AD) and chronic traumatic encephalopathy (CTE). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Transactive response DNA-binding protein of 43 kDa (TDP-43) and tau proteins play critical roles in neurodegenerative diseases, particularly frontotemporal lobar degeneration (FTLD) and Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyotrophic lateral sclerosis (ALS) and Huntington disease (HD) are lethal neurodegenerative diseases affecting motor function. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Repulsive guidance molecule-a (RGMa) has emerged as a significant therapeutic target in a variety of neurological disorders, including neurodegenerative diseases and acute conditions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
246 older adults (mean age = 58.84 ± 7.00 years; 38.21 % males) were included in our data analysis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Patient inclusion started in January 2023, and study enrollment of patients is expected to finish in the second quarter of 2027, whereas the main results are expected to be published in the first quarter of 2028. 5 key findings →
Design: cross-sectional Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia with Lewy bodies (DLB) is the second commonest cause of neurodegenerative dementia in older people. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA) are adult onset neurodegenerative disorders characterised by prominent intracellular α-synuclein aggregates (α-synucleinopathies). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These data reveal a link between reduced glucocerebrosidase and the development of α-synucleinopathy and pathophysiological abnormalities in mice, and support the development of GCase therapeutics to reduce α-synucleinopathy in PD and related disorders. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Selective loss of neurons, abnormal protein deposition and neuroinflammation are the common pathological features of neurodegenerative diseases, and these features are closely related to one another. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 2,453 studies in this tag, 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.
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 →