Dementia associated with PD has 2 major pathologic subgroups: neocortical synucleinopathy and neocortical synucleinopathy with Aβ deposition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Dementia associated with PD has 2 major pathologic subgroups: neocortical synucleinopathy and neocortical synucleinopathy with Aβ deposition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), sporadic multisystem tauopathy, and some forms of frontotemporal dementia with Parkinsonism linked to chromosome 17 are characterized by neuronal and glial lesions accumulating tau protein containing 4 conserved repeats in microtubule-binding domain (4R tau). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal lobar degenerations are a group of disorders characterized by circumscribed degeneration of the frontal and temporal lobes and diverse histopathologic features. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal dementia with parkinsonism (FTDP) is a major neurodegenerative syndrome, particularly for those with symptoms beginning before age 65 years. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A group of similar autosomal dominant hereditary neurodegenerative disorders have been linked to chromosome 17 in thirteen kindreds. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The term oligomeropathies defines the neurodegenerative disorders associated with protein misfolding, where small soluble aggregates (oligomers 4-200 KDa) are the cause of neuronal dysfunction and are responsible for spreading the pathology. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The primary feature of dementia with Lewy bodies (DLB) is the aggregation of alpha-synuclein into characteristic lesions: Lewy bodies (LBs) and Lewy neurites. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We investigated by immunohistochemistry the deposition of alpha-synuclein in the brains of deceased patients with the parkinsonism-dementia complex (PDC) of Guam. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease (PD) and dementia with Lewy bodies (DLB) share clinical and pathological similarities. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Falls are common in Parkinson's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease (PD) and dementia with Lewy bodies (DLB) are among the human synucleinopathies, which show alpha-synuclein immunoreactive neuronal and/or glial aggregations and progressive neuronal loss in selected brain regions (eg, substantia nigra, ventral tegmental area, pedunculopontine nucleus). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dopamine loss in the substantia nigra causes several of the motor signs seen in Parkinson's disease, but there is now increasing evidence highlighting the importance of cholinergic loss in the pathophysiology of nonmotor symptoms. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Navigate PD was an educational program established to supplement existing guidelines and provide recommendations on the management of Parkinson's disease (PD) refractory to oral/transdermal therapies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The discovery of C9orf72 mutations as the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) has awakened a surge of interest in deciphering how mutations in this mysterious gene cause disease and what can be done to stop it. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
One hundred patients with Parkinson's disease (PD) and five patients with progressive supranuclear palsy were questioned about the frequency, circumstances, and consequences of falling. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The management of Parkinson's disease (PD) tends to focus on the presenting motor syndrome; yet, in the long term, nonmotor complications of the illness and complications of treatment become increasingly troublesome. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Degenerative diseases of the basal ganglia, such as Huntington's disease (HD), Parkinson's disease, and Wilson's disease, are characterized by motor, cognitive, and psychiatric manifestations. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although falls are known to occur in several parkinsonian disorders, such as Parkinson's disease (PD), multiple system atrophy (MSA), dementia with Lewy bodies (DLB), corticobasal degeneration (CBD), and progressive supranuclear palsy (PSP), differences in the evolution of this feature have not been studied systematically in pathologically confirmed cases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The mild cognitive impairment (MCI) stage of dementia with Lewy bodies (MCI-DLB) has not yet been defined, but is likely to differ in the MCI stage of Alzheimer's disease (MCI-AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We report the clinical features of the original Chilean family with Kufor-Rakeb syndrome (KRS) that led to the discovery of the ATP13A2 gene at the PARK9 locus. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Both groups have extensive sleep problems. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Opinion statement Parkinson's disease (PD) has been increasingly recognized as having a multitude of nonmotor symptoms including psychosis, cognitive impairment and dementia, mood disturbances, fatigue, apathy, and sleep disorders. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyotrophic lateral sclerosis (ALS), first described by Jean-Martin Charcot in the 1870s, is an age-related disorder that leads to degeneration of motor neurons. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Despite calls for improved access to palliative care for people with Parkinson's disease, services have been slow in developing. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing evidence suggests that synaptic dysfunction is a key pathophysiological hallmark in neurodegenerative disorders, including Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 1,021 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 27,780 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.
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 →