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Find studies

Showing 26–50 of 107 studies with an author at Sapienza University of Rome (IT) (page 2 of 5) · 27,780 in the whole library · How the 0–100 score works

Download bibliography of these 107 studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

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

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.

Mapping distributed sources of cortical rhythms in mild Alzheimer's disease. A multicentric EEG study

✓ Peer-reviewed alzhub usefulness score 51 out of 100. NeuroImage 2004-05-01

The study aimed at mapping (i) the distributed electroencephalographic (EEG) sources specific for mild Alzheimer's disease (AD) compared to vascular dementia (VaD) or normal elderly people (Nold) and (ii) the distributed EEG sources sensitive to the mild AD at different stages of severity. 4 key findings →

Evidence: low

In the last few years, co-ultramicronized palmitoylethanolamide combined with luteoline has emerged as a potential therapeutic molecule in neurodegenerative disorders pathogenically related to frontotemporal dementia, for its demonstrated strong anti-inflammatory and neuroprotective properties. 4 key findings →

Design: clinical trial Participants: 25 Evidence: high

Clinical and experimental evidence suggest that dopaminergic transmission is impaired in FTD. 2 key findings →

Participants: 128 Evidence: high

The alteration of the insulin-signaling/mTOR pathways represents an early event in DS brain and likely contributes to the cerebral dysfunction and intellectual disability observed in this unique population. 1 key finding →

Participants: 17 Evidence: low

The clinical symptoms of Alzheimer disease (AD) include a gradual memory loss and subsequent dementia, and neuropathological deposition of senile plaques and neurofibrillary tangles. 5 key findings →

Evidence: low

Transcranial magnetic stimulation (TMS) is a powerful tool to probe in vivo brain circuits, as it allows to assess several cortical properties such asexcitability, plasticity and connectivity in humans. 1 key finding →

Evidence: low

Emotion recognition progresses from a deficit in low-intensity fearful facial recognition in a-MCI phase to a deficit in all intensities and emotions in mild AD. 2 key findings →

Design: case-control study Evidence: moderate

Most studies suggest depression may contribute to neurodegeneration, but clinical, neuroimaging, and longitudinal evidence also support its role as a prodrome or consequence, indicating a bidirectional relationship. 2 key findings →

Design: longitudinal study Evidence: moderate

In the initial kindred of ten affected Italian individuals (mean age of disease onset 59·8 years [SD 8·7]), we detected significant linkage of Parkinson's disease to chromosome 14 and nominated LRP10 as the disease-causing gene. 2 key findings →

Evidence: low

Neuroinflammation plays a pivotal role in Alzheimer's disease (AD) and Parkinson's disease (PD), the leading causes of dementia. 4 key findings →

Evidence: low

Nutrition and Lifestyle Interventions in Managing Dyslipidemia and Cardiometabolic Risk

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Nutrients 2025-02-23

Dyslipidemia, characterized by abnormal blood lipid levels, is a major public health concern due to its association with atherosclerotic cardiovascular disease (ASCVD) and other cardiometabolic disorders. 5 key findings →

Evidence: low

What we eat is a cornerstone of cardiovascular disease (CVD) prevention, but health professionals may not have a clear understanding of the current evidence-based research to underpin eating habits and recommendations. 2 key findings →

Evidence: low

Oxidative stress has been implicated in the pathogenesis of a number of diseases including Alzheimer's disease (AD). 1 key finding →

Evidence: low

Although epidemiological data associate hypertension with a strong predisposition to develop Alzheimer disease, no mechanistic explanation exists so far. 4 key findings →

Evidence: low

While educational disparities in dementia incidence are well-known, whether and to what extent they persist beyond dementia onset is less explored. 4 key findings →

Design: longitudinal study Evidence: moderate

Alzheimer disease (AD) is the most common form of dementia among the elderly and is characterized by progressive loss of memory and cognition. 3 key findings →

Evidence: low

These findings demonstrate that chronic InRapa administration is able to exert a neuroprotective effect on Ts65Dn hippocampus by reducing AD pathological hallmarks and by restoring protein homeostasis, thus ultimately resulting in improved cognition. 5 key findings →

Evidence: low

The RNA-binding proteins TDP-43 and FUS form abnormal cytoplasmic aggregates in affected tissues of patients with amyotrophic lateral sclerosis and frontotemporal lobar dementia. 4 key findings →

Evidence: low

Alzheimer's disease (AD), a primary cause of dementia in the aging population, is characterized by extracellular amyloid-beta peptides aggregation, intracellular deposits of hyperphosphorylated tau, neurodegeneration and glial activation in the brain. 4 key findings →

Evidence: low

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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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.

1,034 records (3.7% 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 →

Newest studies, as a dated timeline →    Atom feed