The phosphodiesterase inhibitor, ibudilast, has many effects on lymphocytes, endothelial cells, and glial cells. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Research
29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Dementia prevalence increases with age and Alzheimer's disease (AD) accounts for up to 75% of cases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Human immunodeficiency virus type 1 (HIV-1) infection of the central nervous system (CNS) can result in neurological dysfunction with devastating consequences in a significant proportion of individuals with acquired immune deficiency syndrome. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Accumulating evidence supports a role of chemokines and their receptors in brain function. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Infection with the human immunodeficiency virus (HIV) is associated with a syndrome of cognitive and motor abnormalities that may develop in the absence of opportunistic infections. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
In 4 cases of Parkinson's disease (PD), 2 cases of Dementia with Lewy bodies (DLB) and 3 age-matched controls, the TUNEL/ISEL method was used to detect DNA fragmentation in substantia nigra locus coeruleus and cerebral cortex [method by Gold et al. In addition, immunohistochemistry was performed for an array of apoptosis-related proteins, i.e. the recently described apoptosis specific protein cJun/AP1 (ASP), the proto-oncogenes c-Jun, c-Jun AP1, Bcl2, Bax, Bcl-x, p53, CD 95 (Fas/Apo-1) 4 key findings →
Evidence: low
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Higher ADI was significantly associated with increased CRP (r=0.469, p = 0.002) and TREM-1 (r=0.316, p = 0.047). 5 key findings →
Design: cross-sectional Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The dominant research paradigm for Alzheimer's disease has focused on amyloid-beta plaqueremoval for over three decades, producing no curative therapy despite billions of dollars ofinvestment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Progress in understanding the complexity of Alzheimer's disease informs the search for combination therapies that can successfully prevent or substantially slow the progression of the disease. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer’s disease (AD) is the most widespread neurodegenerative disorder and a leading cause of dementia seen in clinical practice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) is the most common form of dementia affecting more than 6 million people in the United States. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is a major health issue of global concern whereby there are minimal treatment options. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers hold significant promise for the early detection and diagnosis of Alzheimer’s disease (AD) and other dementias. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent advances in dementia research have expanded our understanding of modifiable risk factors, with air pollution being a well-established contributor. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
• The new CB 2 antagonist PGN36 is able to cross the Blood-Brain Barrier. • PGN36 treatment effectively alleviates TAU P301L -induced cognitive decline . • PGN36 is able to reduce TAU protein expression levels and restore synaptic plasticity. • PGN36 modulates TAU P301L -induced pyroptosis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
41/100
The developmental origin of Alzheimer disease (AD) has been proposed but is arguably debated. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Perspectivas futuras O mesmo princípio de modulação glial pode ser aplicado em cenários de morte clínica (parada cardiorrespiratória). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This diploma thesis presents the work carried out during 6 months within the Laboratory directed by Professor Millet, written under the supervision and with the support of Dr. Benjamin Tournier and Silvia Braconi Quintaje. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) affects over 55 million people worldwide and lacks effective disease-modifying therapies targeting neuroinflammation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Emerging evidence indicates that globus pallidus (GP) function can be modulated by orexin-A in movement disorders, while its role in Alzheimer’s disease (AD) and dementia with Lewy bodies (DLB) remains unclear. 4 key findings →
Participants: 25 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Compared with stage 0 CKM syndrome, stages 3 and 4 were significantly associated with an increased risk of dementia (hazard ratio [HR], 1.35; 95% confidence interval [CI], 1.14-1.59; HR, 1.80; 95% CI 1.57-2.07). 5 key findings →
Participants: 389,287 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Semantic dementia (SD) is a clinical subtype of frontotemporal dementia characterized by impaired word comprehension and semantic memory, and occurs nearly always sporadically. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
TDP-43 seeding activity was detected in 67% of TDP-43-linked symptomatic patients, with a specificity of 93%. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
41/100
While neuropathological and genetic studies have established the crucial involvement of TDP-43 proteinopathy in the pathogenesis of amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and related neurodegenerative disorders, multiple studies have described the presence of TDP-43 inclusions in muscular disorders, including inclusion body myositis but also other related rimmed vacuole myopathies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal dementia (FTD) is a group of early onset and progressive disorders, characterized by degeneration in the frontal and temporal lobes, and subsequent deterioration in cognition, personality, social behavior, and language, with aggregates of the RNA-binding protein TDP-43 being present in ~45% of the cases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
10 of the 8,203 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.
- Activated microglial exosomes enhance α-Synuclein internalization and accelerate neurodegeneration in lewy body dementia
- Progranulin Gene Therapy Improves Lysosomal Dysfunction and Microglial Pathology Associated with Frontotemporal Dementia and Neuronal Ceroid Lipofuscinosis
- From Stroke to Dementia: a Comprehensive Review Exposing Tight Interactions Between Stroke and Amyloid-β Formation
- The role of abnormal mitochondrial dynamics in the pathogenesis of Alzheimer's disease
- Microglial activatory (immunoreceptor tyrosine-based activation motif)- and inhibitory (immunoreceptor tyrosine-based inhibition motif)-signaling receptors for recognition of the neuronal glycocalyx
- Plasma neurofilament light links mortality to neuroaxonal injury beyond clinical decline and Alzheimer disease plasma biomarkers: a multi-cohort study of oldest old individuals
- Neuroinflammation and Functional Connectivity in Alzheimer's Disease: Interactive Influences on Cognitive Performance
- Testing a MultiTEP-based combination vaccine to reduce Aβ and tau pathology in Tau22/5xFAD bigenic mice
- Pathogenesis, diagnostics, and therapeutics for Alzheimer's disease: Breaking the memory barrier
- Microglia-Mediated Synapse Loss in Alzheimer's Disease
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 29,780 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.
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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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 (3.5% 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 →