Quality of life is dramatically affected in advanced PD patients. 3 key findings →
Evidence: moderate
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.
48/100
Pathological studies have demonstrated abnormalities in white matter that may appear normal on brain imaging. 3 key findings →
Participants: 429 Evidence: low
Full summary, score breakdown and related studies → Original source
Enlarged perivascular spaces are associated with age, lacunar stroke subtype and white matter lesions and should be considered as another magnetic resonance imaging marker of cerebral small vessel disease. 3 key findings →
Participants: 298 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and vascular dementia (VaD) are the two most common forms of dementia. 1 key finding →
Participants: 800,000 Evidence: low
Full summary, score breakdown and related studies → Original source
Biomarkers are urgently needed for the diagnosis and monitoring of disease progression in Parkinson's disease. 5 key findings →
Participants: 117 Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies of neurological diseases have identified thousands of variants associated with disease phenotypes. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
48/100
Patients with Alzheimer's disease (AD) and Parkinson's disease (PD) often have overlap in clinical presentation and brain neuropathology suggesting that these two diseases share common underlying mechanisms. 1 key finding →
Participants: 80 Evidence: low
Full summary, score breakdown and related studies → Original source
Recent studies indicate that the adaptive immune system plays a role in Lewy body dementia (LBD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
48/100
In Alzheimer's disease, tau pathology spreads hierarchically from the inferior temporal lobe throughout the cortex, ensuing cognitive decline and dementia. 4 key findings →
Participants: 55 Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in the CHCHD10 gene have been recently identified in a large family with a complex phenotype variably associating frontotemporal dementia (FTD) with amyotrophic lateral sclerosis (ALS), cerebellar ataxia, myopathy, and hearing impairment. 1 key finding →
Participants: 115 Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease (PD), following Alzheimer's disease, is the second-most common neurodegenerative disorder in the United States. 5 key findings →
Participants: 630,000 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma neurofilament light chain (NfL) is a marker of neuronal damage in different neurological disorders and might predict disease progression in dementia with Lewy bodies (DLB). 2 key findings →
Participants: 45 Evidence: low
Full summary, score breakdown and related studies → Original source
The proteomic profile discriminated DLB and PD from NC with an AUC (Area Under the Curve) of 0.96 with demographics of age, sex and education. 4 key findings →
Participants: 89 Evidence: low
Full summary, score breakdown and related studies → Original source
48/100
Reduced speed and reduced smoothness in speed and pressure were observed particularly in the LBD group, while increased pauses and total durations were observed in both the AD and LBD groups. 3 key findings →
Participants: 47 Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with suspected AD neuropathology (Aβ-positive patients with mild cognitive impairment or AD dementia) showed high-intensity temporoparietal cortex-predominant [18F]PI-2620 binding. 5 key findings →
Participants: 65 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and vascular dementia (VaD) are the two commonest causes of dementia in older adults and frequently coexist as mixed neurodegenerative-cerebrovascular pathology. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
We included 110 patients with CAA (strictly lobar ICHs/CMBs), 33 with HA (strictly deep ICHs/CMBs) and 97 with mixed lobar/deep ICHs/CMBs. 5 key findings →
Participants: 110 Evidence: low
Full summary, score breakdown and related studies → Original source
We used an autopsy series to determine whether the newest dementia with Lewy bodies (DLB) consensus pathologic classification correlates with premortem diagnosis of DLB. 1 key finding →
Participants: 95 Evidence: low
Full summary, score breakdown and related studies → Original source
48/100
There is increasing interest in studying retinal biomarkers for various neurodegenerative diseases. 2 key findings →
Participants: 99 Evidence: low
Full summary, score breakdown and related studies → Original source
In both databases, total healthcare resource utilization and costs increased with number of core features. 4 key findings →
Participants: 536 Evidence: low
Full summary, score breakdown and related studies → Original source
Hippocampal atrophy detected by volumetric MRI is a sensitive feature of early Alzheimer's disease (AD), but there are no studies evaluating hippocampal atrophy by MR volumetry in other dementing diseases. 2 key findings →
Participants: 113 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD), non-AD dementia, and Parkinson's disease (PD) are increasingly common in older adults, yet all risk factors for their onset are not fully understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The predefined superiority of donepezil to the placebo was not confirmed in either active group in the primary analysis. 5 key findings →
Participants: 142 Evidence: low
Full summary, score breakdown and related studies → Original source
We investigated whether the cerebrospinal fluid (CSF) biomarkers beta-amyloid 1-42 (Abeta1-42), total tau (t-tau) protein and tau protein phosphorylated at threonine 181 (p-tau181) could discriminate Alzheimer's disease (AD) from vascular dementia (VD) patients. 4 key findings →
Participants: 35 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and vascular dementia (VaD) are intertwined by mixed dementia (MD) harboring varying degrees of AD pathology in combination with cerebrovascular disease. 5 key findings →
Participants: 30 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.
- Transgenic mice carrying a human mutant superoxide dismutase transgene develop neuronal cytoskeletal pathology resembling human amyotrophic lateral sclerosis lesions
- β-Amyloid PET and neuropathology in dementia with Lewy bodies
- Frontotemporal dementia associated CHCHD10V57E mutation aggravates tau pathology via disrupting the CHCHD10-Rab7A-TBC1D15 complex
- Initial cognitive decline is associated with cortical thinning in early Parkinson disease
- Inclusion formation and neuronal cell death through neuron-to-neuron transmission of alpha-synuclein
- Environmental risk factors for all-cause dementia, Alzheimer's disease dementia, vascular dementia, and mild cognitive impairment: An umbrella review and meta-analysis
- Executive function in progressive and nonprogressive behavioral variant frontotemporal dementia
- The neuropathology of chronic traumatic encephalopathy
- Interleukin-1 mediates Alzheimer and Lewy body pathologies
- Cognitive impairment in Parkinson's disease and dementia with Lewy bodies
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 →