Microglial activation is an early and common feature of almost all neuropathologies, including multiple sclerosis, Alzheimer's disease and mechanical injury.
Full summary, score breakdown and related studies → Original source Free full text
Research
28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Mutations in the presenilin genes are the main cause of familial Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the healthy adult brain synapses are continuously remodelled through a process of elimination and formation known as structural plasticity. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
See Attems and Jellinger (doi:10.1093/brain/awx360) for a scientific commentary on this article. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a heterogeneous disorder with multiple etiologies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Familial forms of frontotemporal dementia (FTD) with tauopathy are mostly caused by mutations in the gene encoding the microtubule-associated protein tau (MAPT). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies are a diverse group of progressive and fatal neurodegenerative diseases characterized by aberrant tau inclusions in the central nervous system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although multiple CHCHD10 mutations are associated with the spectrum of familial and sporadic frontotemporal dementia-amyotrophic lateral sclerosis (FTD-ALS) diseases, neither the normal function of endogenous CHCHD10 nor its role in the pathological milieu (that is, TDP-43 pathology) of FTD/ALS have been investigated. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recently intronic and exonic mutations in the Tau gene have been found to be associated with familial neurodegenerative syndromes characterized not only by a predominantly frontotemporal dementia but also by the presence of neurological signs consistent with the dysfunction of multiple subcortical neuronal circuitries. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An unusually high frequency of atypical Parkinson syndrome has been delineated over the last 5 years in the French West Indies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Systemic inflammation can impair cognition with relevance to dementia, delirium and post-operative cognitive dysfunction. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease dementia (PDD) and dementia with Lewy bodies (DLB) are clinically and neuropathologically highly related α-synucleinopathies that collectively constitute the second leading cause of neurodegenerative dementias. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Epidemiological studies show that individuals who carry the relatively uncommon APOE ε2 allele rarely develop Alzheimer disease, and if they do, they have a later age of onset, milder clinical course, and less severe neuropathological findings than people without this allele. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genetic mutations in the tau gene on chromosome 17 are known to cause frontotemporal dementias. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A 59-year-old man developed problems with reading and driving. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Detailed molecular pathology studies and clinicopathological phenotyping of familial amyotrophic lateral sclerosis (FALS) with characterised mutations in the gene encoding Cu/Zn superoxide dismutase (SOD1) will yield important insights into the pathogenesis of motor neuron degeneration. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Prostate cancer (PCa) is one of the most prevalent malignancies affecting males worldwide. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Memory loss in Alzheimer's disease (AD) is attributed to pervasive weakening and loss of synapses. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic dysfunction plays a central role in Alzheimer's disease (AD), since it drives the cognitive decline. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early life experience influences stress reactivity and mental health through effects on cognitive-emotional functions that are, in part, linked to gene expression in the dorsal and ventral hippocampus. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Major Depressive Disorder (MDD) is a common psychiatric disorder for which available medications are often not effective. 4 key findings →
Participants: 23 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease (cSVD) comprises pathological processes of the small vessels in the brain that may manifest clinically as stroke, cognitive impairment, dementia, or gait disturbance. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A diffusion prepared 3D GRASE pCASL sequence with TGV regularized SPA modeling was proposed to measure BBB water permeability noninvasively with good reproducibility. k w may serve as an imaging marker of cerebral SVD and associated cognitive impairment. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
IR among asymptomatic APOEɛ4 carriers was associated with higher P-Tau181 and T-Tau in late-middle age. 5 key findings →
Participants: 113 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid plaques and tau tangles are the hallmark pathologic features of Alzheimer's disease (AD). 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 7,799 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.
- Metal dyshomeostasis and oxidative stress in Alzheimer's disease
- Anti-Aβ Antibody Aducanumab Regulates the Proteome of Senile Plaques and Closely Surrounding Tissue in a Transgenic Mouse Model of Alzheimer’s Disease
- α-Synuclein BAC transgenic mice exhibit RBD-like behaviour and hyposmia: a prodromal Parkinson's disease model
- Presenilin Is Essential for ApoE Secretion, a Novel Role of Presenilin Involved in Alzheimer's Disease Pathogenesis
- Altered Mitochondrial DNA Methylation Pattern in Alzheimer Disease-Related Pathology and in Parkinson Disease
- Neuroimaging correlates of HIV-associated BBB compromise
- TREM2 expression level is critical for microglial state, metabolic capacity and efficacy of TREM2 agonism
- Genetic, Transcriptome, Proteomic, and Epidemiological Evidence for Blood-Brain Barrier Disruption and Polymicrobial Brain Invasion as Determinant Factors in Alzheimer's Disease
- The relationships between neuroinflammation, beta-amyloid and tau deposition in Alzheimer's disease: a longitudinal PET study
- Age-dependent behavioral and biochemical characterization of single APP knock-in mouse (APPNL-G-F/NL-G-F) model of 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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.
1,038 records (3.6% of the library) are not peer-reviewed — 966 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 →