For decades, astrocytes have been regarded as passive partners of neurons in central nervous system (CNS) function. 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.
Sphingosine-1-phosphate (S1P) and S1P receptors (S1PR) are ubiquitously expressed. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The importance of TANK binding kinase-1 (TBK1), a multimeric kinase that modulates inflammation and autophagy, in human health has been highlighted for the first time by the recent discoveries of mutations in TBK1 that underlie amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), normal tension glaucoma (NTG) or childhood herpes simplex encephalitis (HSE). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Reactive microgliosis, hallmark of neuroinflammation, may contribute to neuronal degeneration, as shown in several neurodegenerative diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The immune system is now considered a major factor in Alzheimer Disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease (AD) is a neurodegenerative condition characterized by the formation of amyloid-β plaques, aggregated and hyperphosphorylated tau protein, activated microglia and neuronal cell death, ultimately leading to progressive dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Two basic discoveries have spurred research into inflammation as a driving force in the pathology of Alzheimer disease (AD). 4 key findings →
Evidence: low
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Cerebral vascular amyloid beta-protein (Abeta) deposition, also known as cerebral amyloid angiopathy, is a common pathological feature of Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Participants' age ranged from 45 to 87, 53% were women, and 26% were diagnosed with dementia (39% AD, 18% Lewy Body and 17% Frontotemporal Dementia; Table 1). 5 key findings →
Design: cross-sectional Participants: 255 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Systemic inflammatory biomarkers were primarily associated with age/socio-demographic characteristics, remained strikingly stable over time, and were not associated with AD progression. 5 key findings →
Participants: 333 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BackgroundSystemic inflammation has been implicated in cognitive aging and neurodegeneration; however, inflammatory biomarkers are expressed in coordinated patterns rather than as isolated markers. 4 key findings →
Design: cross-sectional Participants: 334 Evidence: moderate
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Sortilin (SORT1) is a lipoprotein receptor that shows genome-wide association with hypercholesterolaemia, explained by its ability to control hepatic output of lipoproteins. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer’s disease (AD) is a heterogeneous neurodegenerative disorder in which tau neurofibrillary tangles are a pathological hallmark closely associated with cognitive dysfunction and neurodegeneration. 5 key findings →
Participants: 615 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Overall PiB-PET uptake increased during the first two years (before ARIA-E) and decreased during the last two years (including ARIA-E episodes) (0.03±0.05 vs. -0.04±0.04 SUVR/year, p-value=0.01, Figure 2). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Atherosclerosis is a progressive, multifactorial disease driven by the interplay of lipid dysregulation, chronic inflammation, oxidative stress, and maladaptive vascular remodeling. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease and its clinical variants have characteristic spatial and temporal progression patterns of amyloid and tau driving symptomatology, but the distribution of microglia density, as measured by 18kDa translocator protein (TSPO) PET, is unknown. 5 key findings →
Design: longitudinal study Evidence: moderate
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We demonstrate that senolytic treatment is an effective therapeutic strategy to mitigate cognitive impairment by reducing neuroinflammation and associated metabolic disturbances. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
44/100
Vascular dementia (VaD) is a heterogeneous group of brain disorders caused by cerebrovascular pathologies and the second most common cause of dementia, accounting for over 20% of cases and posing an important global health concern. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
44/100
Cerebrolysin (CBL) is a combination of neurotrophic peptides and amino acids derived from pig brains. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mutations in the TARDBP gene encoding TDP-43 protein are linked to loss of function in neurons and familial frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Forty bvFTD patients and 40 HC (56.25% female, mean age of 63.55 years) were involved. 5 key findings →
Participants: 36 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings establish IF as a potent modulator of synaptic resilience in VaD, acting through coordinated preservation of synaptic structure, inhibition of inflammatory synapse loss, and metabolic reprogramming. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD) are two neurodegenerative disorders that share common genes and pathomechanisms and are referred to as the ALS-FTD spectrum. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
TDP-43 mislocalization and aggregation are key pathological features of amyotrophic lateral sclerosis (ALS)- and frontotemporal dementia (FTD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
44/100
The most common clinical symptoms in FTLD-TDP-PSP were memory loss (100%) followed by parkinsonism (80%), early falls (60%), and behavioral variant FTD (60%). 5 key findings →
Participants: 270 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.
- TRPMLs and TPCs: Targets for lysosomal storage and neurodegenerative disease therapy?
- Triggering receptor expressed on myeloid cells 2 (TREM2) promotes adipogenesis and diet-induced obesity
- Dopamine neuronal loss contributes to memory and reward dysfunction in a model of Alzheimer's disease
- Neurofilament Biomarkers in Neurology: From Neuroinflammation to Neurodegeneration, Bridging Established and Novel Analytical Advances with Clinical Practice
- Corticobasal degeneration: a pathologically distinct 4R tauopathy
- The impact of nutrition on COVID-19 susceptibility and long-term consequences
- TREM2 Regulates the Removal of Apoptotic Cells and Inflammatory Processes during the Progression of NAFLD
- Neuropathological Mechanisms Associated with Pesticides in Alzheimer’s Disease
- Molecular landscapes of human hippocampal immature neurons across lifespan
- Alzheimer's Disease: Silent Erosion of Memory - From Discovery to Modern Crisis and the Quest for a Cure
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 →