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Research

30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 226–246 of 246 studies (page 10 of 10) · 30,180 in the whole library · How the 0–100 score works

Download bibliography of these 246 studies, in this order: BibTeX (.bib) · RIS (.ris)

Showing 246 studies tagged autophagy — clear

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

Raman Spectroscopic Characterization of Secondary Structure in Natively Unfolded Proteins: α-Synuclein

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of the American Chemical Society 2004-02-04

The application of Raman spectroscopy to characterize natively unfolded proteins has been underdeveloped, even though it has significant technical advantages. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Histone deacetylases (HDACs) in frontotemporal lobar degeneration

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuropathology and Applied Neurobiology 2015-01-29

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

Frontotemporal Dementia Patient Neurons With Progranulin Deficiency Display Protein Dyshomeostasis

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv : the preprint server for biology 2023-01-20

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

Rab11-exosome biogenesis regulators mediate Aβ-induced intercellular propagation of endolysosomal trafficking defects and neurodegeneration

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-20

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

Disrupting SORL1-retromer endosomal recycling in mice drives the age-dependent neurodegenerative signature of Alzheimer's disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-30

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

The Filamin A Proteomic Switch: Solubility States and Cytoskeletal Dynamics Explain the Inverse Epidemiological Relationship Between Cancer and Alzheimer’s Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-26

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

A Biophysical Framework for Neurodegeneration: Prioritizing Protein Homeostasis Over Aggregate Toxicity

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2025-12-31

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

Early life social isolation primes flies for more rapid TDP-43 dependent neurodegeneration later in life

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-28

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

ALS-associated mutations reveal a conserved C-terminal self-assembly module in the TDP-43 low-complexity domain

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-12

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

Intrastriatal injection of amplified Lewy body dementia (LBD) fibrils in mice results in accumulation of fibrils with LBD structure and neurodegeneration

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-13

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

The Alzheimer’s disease risk gene ABCA7 regulates microglial lysosomal and lipid homeostasis and promotes phagocytosis to maintain neuronal health

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-19

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

From across this tag

9 of the 246 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 9. The same 9 appear here every time.

↑ Change the filters

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 →

Newest studies, as a dated timeline →    Atom feed