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Research

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 13,776–13,800 of 27,146 studies marked Peer-reviewed (page 552 of 1086) · 28,180 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; 13,658 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.

The Lewy body in Parkinson's disease: molecules implicated in the formation and degradation of alpha-synuclein aggregates

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Neuropathology : official journal of the Japanese Society of Neuropathology 2007-10-01

The histological hallmark of Parkinson's disease (PD) is the presence of fibrillar aggregates called Lewy bodies (LBs). 1 key finding →

Evidence: low

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

The role of zinc, copper, manganese and iron in neurodegenerative diseases

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Neurotoxicology 2019-08-01

Metals are involved in different pathophysiological mechanisms associated with neurodegenerative diseases (NDDs), including Alzheimer's disease (AD), Parkinson's disease (PD) and multiple sclerosis (MS). 2 key findings →

Evidence: low

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

Increased levels of 4-hydroxynonenal and acrolein, neurotoxic markers of lipid peroxidation, in the brain in Mild Cognitive Impairment and early Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Neurobiology of aging 2005-07-01

Previous studies show increased levels of lipid peroxidation and neurotoxic by-products of lipid peroxidation including 4-hydroxynonenal (HNE) and acrolein in vulnerable regions of the Alzheimer's disease (AD) brain. 5 key findings →

Evidence: low

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

Redox proteomic identification of 4-hydroxy-2-nonenal-modified brain proteins in amnestic mild cognitive impairment: insight into the role of lipid peroxidation in the progression and pathogenesis of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Neurobiology of disease 2008-01-05

Numerous investigations point to the importance of oxidative imbalance in mediating AD pathogenesis. 5 key findings →

Evidence: low

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

Abnormal salience network in normal aging and in amnestic mild cognitive impairment and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Human brain mapping 2013-11-12

The salience network (SN) serves to identify salient stimuli and to switch between the central executive network (CEN) and the default-mode network (DMN), both of which are impaired in Alzheimer's disease (AD)/amnestic mild cognitive impairment (aMCI). 3 key findings →

Evidence: low

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

Elevated levels of 3-nitrotyrosine in brain from subjects with amnestic mild cognitive impairment: implications for the role of nitration in the progression of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Brain research 2007-03-07

A number of studies reported that oxidative and nitrosative damage may be important in the pathogenesis of Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

Sulcal morphology changes and their relationship with cortical thickness and gyral white matter volume in mild cognitive impairment and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. NeuroImage 2008-07-22

We investigated the changes of sulcal shape (average mean curvature in folded regions and sulcal depth) in mild cognitive impairment (MCI) and Alzheimer's disease (AD) using quantitative surface-based methods in a large sample of magnetic resonance imaging data. 4 key findings →

Evidence: low

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

Mild cognitive impairment in the general population: occurrence and progression to Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry 2008-07-01

Two-thirds of MCI-multidomains, but only half of MCI-amnestic progress to AD. 1 key finding →

Evidence: low

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

Cerebral blood flow measured by arterial spin labeling MRI at resting state in normal aging and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Neuroscience and biobehavioral reviews 2016-11-28

Arterial spin labeling (ASL) magnetic resonance imaging uses arterial blood water as an endogenous tracer to measure cerebral blood flow (CBF). 4 key findings →

Evidence: low

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

Cerebrospinal fluid A beta42 is increased early in sporadic Alzheimer's disease and declines with disease progression

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Annals of neurology 1999-04-01

All mutations known to cause familial Alzheimer's disease (AD) act by increasing the levels of soluble beta-amyloid peptide (A beta), especially the longer form, A beta42. 2 key findings →

Evidence: low

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

Clinical aspects of melatonin intervention in Alzheimer's disease progression

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Current neuropharmacology 2010-09-01

Melatonin secretion decreases in Alzheimer´s disease (AD) and this decrease has been postulated as responsible for the circadian disorganization, decrease in sleep efficiency and impaired cognitive function seen in those patients. 5 key findings →

Evidence: high

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

Defining Alzheimer as a common age-related neurodegenerative process not inevitably leading to dementia

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Progress in neurobiology 2012-03-21

Since the description by Alois Alzheimer, more than 50 years have passed during which senile dementia and pre-senile dementia have been considered Alzheimer disease (AD) on the basis of their common neuropathological and clinical manifestations. 5 key findings →

Evidence: low

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

Progression of tau pathology in cholinergic Basal forebrain neurons in mild cognitive impairment and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The American journal of pathology 2011-09-23

Tau is a microtubule-associated protein that forms neurofibrillary tangles (NFTs) in the selective vulnerable long projection neurons of the cholinergic basal forebrain (CBF) in Alzheimer's disease (AD). 3 key findings →

Evidence: low

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

Four subgroups of Alzheimer's disease based on patterns of atrophy using VBM and a unique pattern for early onset disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. NeuroImage 2006-08-10

To clarify the involvement of the posterior cingulate cortex (PCC) in Alzheimer's disease (AD), we analyzed brain volume loss by voxel-based morphometry. 4 key findings →

Participants: 20 Evidence: low

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

Molecular and cellular pathophysiology of preclinical Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Behavioural brain research 2016-05-13

Although the two pathological hallmarks of Alzheimer's disease (AD), senile plaques composed of amyloid-β (Aβ) peptides and neurofibrillary tangles (NFTs) consisting of hyperphosphorylated tau, have been studied extensively in postmortem AD and relevant animal and cellular models, the pathogenesis of AD remains unknown, particularly in the early stages of the disease where therapies presumably would be most effective. 2 key findings →

Evidence: low

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

Phosphoprotein phosphatase activities in Alzheimer disease brain

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Journal of neurochemistry 1993-09-01

Microtubule-associated protein tau is known to be hyperphosphorylated in Alzheimer disease brain and this abnormal hyperphosphorylation is associated with an inability of tau to promote the assembly of microtubule in the affected neurons. 4 key findings →

Evidence: low

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

Episodic-like memory deficits in the APPswe/PS1dE9 mouse model of Alzheimer's disease: relationships to beta-amyloid deposition and neurotransmitter abnormalities

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Neurobiology of disease 2005-04-01

Transgenic mice made by crossing animals expressing mutant amyloid precursor protein (APPswe) to mutant presenilin 1 (PS1dE9) allow for incremental increases in Abeta42 production and provide a model of Alzheimer-type amyloidosis. 4 key findings →

Evidence: low

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

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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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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