27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
We found a significantly greater intensity of cytoplasmic immunostaining for HDAC4 and HDAC6 in granule cells of the dentate gyrus in cases of FTLD overall compared with controls, and specifically in cases of FTLD tau‐ P icks compared with FTLD tau‐ MAPT and controls. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Haploinsufficiency of progranulin (PGRN) causes frontotemporal dementia (FTD), a devastating neurodegenerative disease with no effective treatment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s Disease (AD) is characterised by two histopathological hallmarks, intracellular tau-containing neurofibrillary tangles and extracellular amyloid plaques containing β-amyloid (Aβ), a specific cleavage product of Amyloid Precursor Protein (APP). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
MRI studies have mapped the atrophic signature that distinguishes Alzheimer's disease (AD), isolating regions differentially vulnerable to its age-dependent neurodegenerative process. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This structural configuration shields the scaffold from calpain-mediated cleavage, reconfiguring FLNA into an active motility engine driving invasive lamellipodia but stalls proteolytic processing and forces an absolute loss of the nuclear FLNA-90 tumor-suppressor brake, unleashing uninhibited c-Myc oncogenic transcription. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lysosomal distribution is critical for numerous biological functions within the cell, including protein degradation in autophagosomes, cholesterol homeostasis, and cell invasion. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neurodegenerative research has long hypothesized that aggregated proteins such as amyloid‑β (Aβ), tau, and α‑synuclein (αSyn) are intrinsically toxic and are directly associated with the etiologies of Alzheimer’s disease (AD) and Parkinson’s disease (PD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Scrapie, a prion disease, is usually considered a protein-only infection. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A key pathophysiological hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is loss of nuclear localization and abnormal cytoplasmic aggregation of TAR DNA-binding protein 43 (TDP-43). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genetic variation in the human gene encoding the lysosomal transmembrane protein 106B (TMEM106B) drives risk of neurodegenerative dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
TAR DNA-binding protein 43 (TDP-43) is an RNA-binding protein whose low-complexity domain (LCD) mediates self-assembly, liquid-liquid phase separation, and pathological aggregation associated with amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 2 key findings →
Participants: 47 Evidence: low
Full summary, score breakdown and related studies → Original source
The defining neuropathologic feature of Lewy body dementia (LBD) and Parkinson’s disease (PD) is alpha-synuclein (Asyn) fibril accumulation in Lewy bodies (LBs) and Lewy neurites (LNs). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
ABCA7-KO iMGs were deficient for proteins involved in lysosome function, measured by down-regulated lysosomal proteomic signatures, as well as reduced DQ-BSA activity and reduced LAMP1+ area. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is characterized by a decline in neuronal proteostasis that favours the accumulation of misfolded proteins. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative proteinopathies are defined by distinct proteins whose folding, trafficking and clearance depend on shared proteostasis machinery. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
9 of the 240 studies in this tag, 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 9. The same 9 appear here every time.
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
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.
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 27,380 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% of the library) are not peer-reviewed — 962 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 →