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Research

30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 2,676–2,700 of 2,834 studies · tagged Other Dementias (page 108 of 114) · 30,980 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these 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.

Subjects

Authors

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

Institutions

From OpenAlex; 16,452 studies have no institution on record and are not counted here.

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.

Portuguese family with the co-occurrence of frontotemporal lobar degeneration and neuronal ceroid lipofuscinosis phenotypes due to progranulin gene mutation

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neurobiology of aging 2016-03-03

We and others have reported heterozygous progranulin mutations as an important cause of frontotemporal lobar degeneration (FTLD). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Electroencephalographic slowing heralds mild cognitive impairment in idiopathic REM sleep behavior disorder

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Sleep medicine 2010-05-11

Our findings suggest that the presence of marked EEG slowing on spectral analysis might be indicative of the short-term development of MCI in patients initially diagnosed with IRBD. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Glucocerebrosidase deficiency accelerates the accumulation of proteinase K-resistant α-synuclein and aggravates neurodegeneration in a Drosophila model of Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Human molecular genetics 2015-09-11

Alpha-synuclein (αSyn) plays a central role in the pathogenesis of Parkinson's disease (PD) and dementia with Lewy bodies (DLB). 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Central mammalian neurons normally resistant to glutamate toxicity are made sensitive by elevated extracellular Ca2+: toxicity is blocked by the N-methyl-D-aspartate antagonist MK-801

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1988-09-01

It is widely held that a glutamate-like toxin that resembles N-methyl-D-aspartate may be responsible for the death of nerve cells seen after severe neurological insults including stroke, seizures, and degenerative disorders, such as Huntington disease, Alzheimer disease, and the amyotrophic lateral sclerosis-parkinsonism-dementia complex found on Guam. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Enhanced ATPase activities as a primary defect of mutant valosin-containing proteins that cause inclusion body myopathy associated with Paget disease of bone and frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Genes to cells : devoted to molecular & cellular mechanisms 2010-07-05

Valosin-containing protein (VCP) has been shown to colocalize with abnormal protein aggregates, such as nuclear inclusions of Huntington disease and Machado-Joseph disease, Lewy bodies in Parkinson disease. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Dissociation of frontotemporal dementia-related deficits and neuroinflammation in progranulin haploinsufficient mice

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2013-03-01

Frontotemporal dementia (FTD) is a neurodegenerative disease with hallmark deficits in social and emotional function. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

New therapeutic strategy for Parkinson's and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Current medicinal chemistry 2010-01-01

The development of potential neuroprotective therapies for neurodegenerative diseases (Parkinson's and Alzheimer's Disease) must be based on understanding their molecular and biochemical pathogenesis. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Imaging amyloid in Parkinson's disease dementia and dementia with Lewy bodies with positron emission tomography

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Movement disorders : official journal of the Movement Disorder Society 2009-01-01

Although Parkinson's disease with later dementia (PDD) and dementia with Lewy bodies (DLB) are pathologically characterized by the presence of intraneuronal Lewy inclusion bodies, amyloid deposition is also associated to varying degrees with both these disorders. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

N-myc and c-myc expression in Alzheimer disease, Huntington disease and Parkinson disease

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Brain research. Molecular brain research 2000-05-01

The present study examines N-myc and c-myc protein expression with Western blotting and single and double-labeling immunohistochemistry in the hippocampus in Alzheimer disease (AD), the striatum in Huntington disease (HD) and the substantia nigra in Parkinson disease (PD). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Amyloid PET Ligands for Dementia

✓ Peer-reviewed alzhub usefulness score 35 out of 100. PET clinics 2010-01-01

The progressive nature of neurodegeneration suggests an age-dependent process that ultimately leads to synaptic failure and neuronal damage in cortical areas of the brain critical for memory and higher mental functions. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

A study of emotional processing in Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Brain and cognition 1998-10-01

This study investigated three aspects of processing materials with emotional content in patients with idiopathic Parkinson's disease (PD): the ability to produce affective prosody, to discriminate affectively loaded speech, and to detect the surprise element in humorous sketches. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Huntington's disease: present treatments and future therapeutic modalities

✓ Peer-reviewed alzhub usefulness score 35 out of 100. International clinical psychopharmacology 2004-03-01

Huntington's disease (HD) is a devastating neuropsychiatric disorder for which therapeutic interventions have been rather fruitless to date, except in a slight symptomatic relief. 3 key findings →

Design: open-label trial Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Total tau in cerebrospinal fluid differentiates Alzheimer's disease from vascular dementia

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Medical science monitor : international medical journal of experimental and clinical research 2003-11-01

Tau protein is a microtubule-associated protein located in neuronal axons, which has been used in various configurations as a diagnostic marker of degenerative changes in the CNS. 4 key findings →

Participants: 102 Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Application of mini-mental state examination and Montreal Cognitive Assessment in the diagnosis of dementia with Lewy bodies and Alzheimer’s disease

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Applied Neuropsychology Adult 2025-03-21

> 0.05). We observed distinct cognitive performances in subjects from both the DLB and AD groups across different stages of dementia. 2 key findings →

Participants: 66 Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Mitochondrial Reactive Oxygen Species Production in Vascular Dementia Following Experimental Diabetes

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Cells 2025-08-15

Type 1 diabetes (T1D) is a serious disease which affects millions of people worldwide and is a major factor for vascular contributions to cognitive impairment and dementia (VCID). 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Hippocampal mitophagy alterations in MAPT-associated frontotemporal dementia with parkinsonism

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Acta Neuropathologica Communications 2025-02-24

The enzyme pair PINK1 and PRKN together orchestrates a cytoprotective mitophagy pathway that selectively tags damaged mitochondria with phospho-serine 65 ubiquitin (pS65-Ub) and directs them for autophagic-lysosomal degradation (mitophagy). 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Graph Spectral Analysis Using Electroencephalography in Alzheimer Disease and Frontotemporal Dementia Patients

✓ Peer-reviewed alzhub usefulness score 35 out of 100. International Journal of Neural Systems 2025-06-12

Graph theory has proven to be useful in studying brain dysfunction in Alzheimer’s disease using MagnetoEncephaloGraphy (MEG) and fMRI signals. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Co‐localization of tau and TDP ‐43 after extracellular vesicle delivery to cells

✓ Peer-reviewed alzhub usefulness score 35 out of 100. FEBS Journal 2025-11-17

Perturbations in the metabolism of microtubule‐associated protein tau (tau) underlie the pathology of a broad array of dementias, including chronic traumatic encephalopathy, amyotrophic lateral sclerosis (ALS) with cognitive impairment (ALSci) and approximately half of the dementias associated with frontotemporal lobar degeneration. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

SHP2 in microglia attenuates neuroinflammation and cognitive deficits in vascular dementia by modulating the FAK/Src/PU. 1/IRF8 pathway

✓ Peer-reviewed alzhub usefulness score 35 out of 100. European journal of medical research 2026-03-31

Vascular dementia is a common cognitive disorder that is often triggered by neuroinflammatory responses caused by cerebrovascular injury, which further exacerbates the progression of the disease. 1 key finding →

Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

From across this tag

10 of the 2,831 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.

↑ 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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.

1,042 records (3.4% of the library) are not peer-reviewed — 967 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    Where this research is being discussed: events