Dementia is a syndrome characterised by chronic, multi-domain, acquired cognitive impairment that causes significant functional limitations. 2 key findings →
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.
The differentiation of subtypes of primary progressive aphasia (PPA) remains challenging. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genetically predisposition to longer educational attainment and harder math class taken were associated with significantly lower statistical odds ratio of ALS. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Locus Coeruleus (LC) is the main noradrenergic nucleus of the central nervous system, and its neurons widely innervate the whole brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Small vessel disease (SVD) refers to conditions where damage to arterioles and capillaries is predominant, leading to reduced, or interrupted perfusion of the affected organ. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The arteriosclerosis-dependent alteration of brain perfusion is one of the major determinants in small vessel disease, since small vessels have a pivotal role in the brain's autoregulation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease (SVD) refers to a group of disease conditions affecting the cerebral small vessels, which include the small arteries, arterioles, capillaries, and postcapillary venules in the brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy is diagnosed in stroke units after lobar intracerebral hemorrhage. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In recent years, studies have demonstrated that hypertension-related changes (e.g., small vascular lesions, inflammatory reactions, hypoperfusion, oxidative stress, damage to autoregulatory processes and the blood-brain barrier, and cerebral amyloid angiopathy) can occur over time in cerebral small vessels, potentially leading to lower cognitive function when blood pressure (BP) control is poor or lacking. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
A neurodegenerative disorder displaying an altered α-synuclein (αS) in the brain tissue is called α-synucleinopathy (αS-pathy) and incorporates clinical entities such as Parkinson disease (PD), PD with dementia, dementia with Lewy bodies, and multiple-system atrophy. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Dementia syndromes associated with Lewy bodies are subdivided into dementia with Lewy bodies (DLB), an underdiagnosed cause of dementia in the elderly, and Parkinson disease with dementia (PDD), cognitive impairment appearing in people diagnosed with Parkinson disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The aggregation of α-synuclein (α-syn) has been implicated in the pathogenesis of many neurodegenerative disorders, including Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
TAR DNA binding protein (TDP-43) is a DNA/RNA binding protein whose pathological role in amyotrophic lateral sclerosis (ALS) and frontal temporal lobe dementia (FTLD) via formation of protein aggregates is well established. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In 2017, it was 200 years since James Parkinson published 'An Essay on the Shaking Palsy' and 20 years since α-synuclein aggregation came to the fore. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This review considers whether the Braak hypothesis on protein propagation could account for prion disease, particularly Creutzfeldt-Jakob disease (CJD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
α-synuclein (αSyn) still remains a mysterious protein even two decades after SNCA encoding it was identified as the first causative gene of familial Parkinson's disease (PD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia with Lewy bodies is characterized by α-synuclein accumulation and degeneration of dopaminergic and cholinergic pathways. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The term proteostasis reflects the fine-tuned balance of cellular protein levels, mediated through a vast network of biochemical pathways. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases, such as Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), and Amyotrophic Lateral Sclerosis (ALS), are a complex "family" of pathologies, characterised by the progressive loss of neurons and/or neuronal functions, leading to severe physical and cognitive inabilities in affected patients. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuronal cell death is the main pathological feature of chronic neurodegenerative diseases (NDs) such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Abnormal accumulation of proteins is a hallmark of a variety of neurological diseases including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 4 key findings →
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
Liu et al. (2017) investigated caregiver burden of patients with frontotemporal lobar degeneration (FTD) and dementia with Lewy bodies (DLB), which was compared with caregivers of patients with Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We provide a review of the current literature and discuss our own care practices. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Dementia and Parkinson's disease are incurable neurological conditions. 5 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.
- Transmission of multiple system atrophy prions to transgenic mice
- Dietary antioxidants and other dietary factors in the etiology of Parkinson's disease
- Language functions in Huntington's disease
- PINK1/PARKIN signalling in neurodegeneration and neuroinflammation
- Interaction of metabolic and inflammatory dysregulation on central degeneration and cognitive function in behavioral variant Frontotemporal dementia
- Phosphorylated TDP-43 in Alzheimer's disease and dementia with Lewy bodies
- Sleep disturbances as risk factors for neurodegeneration later in life
- Parkinsonism and impaired axonal transport in a mouse model of frontotemporal dementia
- Association of Plasma GFAP and NfL in Middle-Aged Adults With MRI Markers of Cerebral Small Vessel Disease Later in Life
- Blood Biomarkers for the Diagnosis of Neurodegenerative Dementia: A Systematic Review
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 →