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Research

29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 126–150 of 169 studies with an author at Northwestern University (US) (page 6 of 7) · 29,780 in the whole library · How the 0–100 score works

Download bibliography of these 169 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.

Other institutions

From OpenAlex; 15,255 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.

Locus coeruleus neurofibrillary degeneration in aging, mild cognitive impairment and early Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Neurobiology of aging 2006-03-29

Neurofibrillary degeneration in the nucleus basalis and a loss of its cortical cholinergic projections are prominent components of the neuropathology in Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

The Amyloid Cascade Hypothesis: A Conclusion in Search of Support

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The American journal of pathology 2024-11-10

The amyloid cascade hypothesis as the etiological underpinning of Alzheimer disease (AD) is supported by a large body of literature, the most influential of which are genetic studies of the 1980s and 1990s. Other evidence includes the neuropathology of Down syndrome, apparent toxicity of oligomeric amyloid-β (Aβ), interactions with apolipoprotein E, and the analogy of cardiac amyloidosis. 1 key finding →

Evidence: low

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

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

The role of amyloid precursor protein processing by BACE1, the beta-secretase, in Alzheimer disease pathophysiology

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journal of biological chemistry 2008-07-23

Amyloid plaques, composed of the amyloid beta-protein (Abeta), are hallmark neuropathological lesions in Alzheimer disease (AD) brain. 4 key findings →

Evidence: low

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

Inhibition of glycogen synthase kinase-3 ameliorates β-amyloid pathology and restores lysosomal acidification and mammalian target of rapamycin activity in the Alzheimer disease mouse model: in vivo and in vitro studies

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journal of biological chemistry 2012-11-15

Accumulation of β-amyloid (Aβ) deposits is a primary pathological feature of Alzheimer disease that is correlated with neurotoxicity and cognitive decline. 4 key findings →

Evidence: low

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

Alzheimer disease Abeta production in the absence of S-palmitoylation-dependent targeting of BACE1 to lipid rafts

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journal of biological chemistry 2008-12-12

Alzheimer disease beta-amyloid (Abeta) peptides are generated via sequential proteolysis of amyloid precursor protein (APP) by BACE1 and gamma-secretase. 4 key findings →

Evidence: low

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

Cerebrospinal fluid proteins predict longitudinal hippocampal degeneration in early-stage dementia of the Alzheimer type

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Alzheimer disease and associated disorders 2012-10-01

Biomarkers are needed to improve the sensitivity and accuracy of diagnosis, and also prognosis, in individuals with early Alzheimer disease (AD). 4 key findings →

Design: longitudinal study Evidence: moderate

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

Dissociable spatial topography of cortical atrophy in early‐onset and late‐onset Alzheimer's disease: A head‐to‐head comparison of the LEADS and ADNI cohorts

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Alzheimer s & Dementia 2025-02-01

After controlling for the level of cognitive impairment, we found a double dissociation between AD clinical phenotype and localization/magnitude of atrophy, characterized by predominant neocortical involvement in EOAD and more focal anterior medial temporal involvement in LOAD. 5 key findings →

Evidence: low

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

Primary progressive aphasia: PPA and the language network

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Annals of neurology 2003-01-01

Primary Progressive Aphasia (PPA) is a behaviorally focal dementia syndrome with deterioration of language functions but relative preservation of other cognitive domains for at least the first two years of disease. 2 key findings →

Evidence: low

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

Abeta toxicity in Alzheimer's disease: globular oligomers (ADDLs) as new vaccine and drug targets

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Neurochemistry international 2002-11-01

Over the past several years, experiments with synthetic amyloid-beta peptide (Abeta) and animal models have strongly suggested that pathogenesis of Alzheimer's disease (AD) involves soluble assemblies of Abeta peptides (Trends Neurosci. 24 (2001) 219). 1 key finding →

Evidence: low

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

β-Site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1)-deficient mice exhibit a close homolog of L1 (CHL1) loss-of-function phenotype involving axon guidance defects

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2012-09-17

BACE1 is the β-secretase enzyme that initiates production of the β-amyloid peptide involved in Alzheimer disease. 4 key findings →

Evidence: low

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

Cerebrospinal fluid S100B is elevated in the earlier stages of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Neurochemistry international 2001-11-01

Postmortem demonstration of increased expression of biologically active S100B in Alzheimer's disease (AD) and its relation to progression of neuropathological changes across the cortical regions suggests involvement of this astrocytic cytokine in the pathophysiology of AD. 4 key findings →

Evidence: low

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

Macrophage tropism of human immunodeficiency virus type 1 isolates from brain and lymphoid tissues predicts neurotropism independent of coreceptor specificity

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of virology 2001-11-01

The viral determinants that underlie human immunodeficiency virus type 1 (HIV-1) neurotropism are unknown, due in part to limited studies on viruses isolated from brain. 4 key findings →

Evidence: low

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

Differential neurocognitive network perturbation in amnestic and aphasic Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Neurology 2020-01-22

Despite the presumptive common underlying neuropathology of amyloid plaques and neurofibrillary tangles, the 2 groups displayed 2 different patterns of network perturbation, each concordant with the clinical presentation and the anatomy of neurodegeneration. 2 key findings →

Participants: 14 Evidence: low

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

Youthful memory capacity in old brains: anatomic and genetic clues from the Northwestern SuperAging Project

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of cognitive neuroscience 2013-01-01

The Northwestern University SuperAging Project recruits community dwellers over the age of 80 who have unusually high performance on tests of episodic memory. 1 key finding →

Evidence: moderate

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

In vitro polymerization of tau protein monitored by laser light scattering: method and application to the study of FTDP-17 mutants

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Biochemistry 2000-05-01

Tau polymerization into the filaments that compose neurofibrillary tangles is seminal to the development of many neurodegenerative diseases. 2 key findings →

Evidence: low

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

Statins cause intracellular accumulation of amyloid precursor protein, beta-secretase-cleaved fragments, and amyloid beta-peptide via an isoprenoid-dependent mechanism

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2005-02-17

The use of statins, 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors that block the synthesis of mevalonate (and downstream products such as cholesterol and nonsterol isoprenoids), as a therapy for Alzheimer disease is currently the subject of intense debate. 4 key findings →

Evidence: low

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

B31-13 Circadian Rest-Activity Rhythm and Alzheimer’s Disease Biomarkers in Adults With Down Syndrome

✓ Peer-reviewed alzhub usefulness score 44 out of 100. American Journal of Respiratory and Critical Care Medicine 2026-05-01

These findings suggest that circadian rhythm disruption as measured via 24-hour RAR is associated with plasma and imaging biomarkers of AD in DS. 5 key findings →

Design: cross-sectional Participants: 29 Evidence: low

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

The causal association between resting state intrinsic functional networks and neurodegeneration

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Brain Communications 2025-01-01

None of the genetically proxied functional network features were significantly associated with neurodegenerative outcomes (adjusted P value >0.05), despite sufficient calculated power. 5 key findings →

Participants: 47 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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.

1,037 records (3.5% 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