Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Critical threshold cerebral hypoperfusion causes Alzheimer's disease?

Acta neuropathologica - 1 Jul 1999

de la Torre J C

Abstract excerpt

After nearly a century of inquiry, the cause of Alzheimer's disease (AD) remains to be found. In this review, basic and clinical evidence is presented that assembles and hypothetically explains most of the key pathologic events associated with the development of AD. These pathologic events are triggered in AD by an impaired cerebral perfusion originating in the microvasculature which affects the optimal delivery...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Alzheimer Disease
Share to Blood Flow Velocity
Share to Cerebral Cortex

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cerebrovascular Circulation

Share to Glucose

Share to Microcirculation

Share to Oxygen

Share to Proteins

Source

Identifiers

PMID: 10412794
DOI: 10.1007/s004010051044

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Critical threshold cerebral hypoperfusion causes Alzheimer's disease?PMID 10412794Read ↗

Are Hippocampal Hypoperfusion and ATP Depletion Prime Movers in the Genesis of Alzheimer’s Disease? A Review of Recent Pertinent Observations from Molecular BiologySemantic proximity Read ↗

Are Hippocampal Hypoperfusion and ATP Depletion Prime Movers in the Genesis of Alzheimer’s Disease? A Review of Recent Pertinent Observations from Molecular BiologySemantic proximity Read ↗

Interplay Between Vascular Dysfunction and Neurodegenerative Pathology: New Insights into Molecular Mechanisms and ManagementSemantic proximity Read ↗

Postischemic dementia with Alzheimer phenotype: selectively vulnerable versus resistant areas of the brain and neurodegeneration versus β-amyloid peptide.Semantic proximity Read ↗

Mechanism of Metabolic Disorder and Endothelial Dysfunction in Alzheimer’s DiseaseSemantic proximity Read ↗

Mechanism of Metabolic Disorder and Endothelial Dysfunction in Alzheimer’s DiseaseSemantic proximity Read ↗

Current insights into molecular mechanisms of Alzheimer disease and their implications for therapeutic approaches.Semantic proximity Read ↗

Multiple substrates of late-onset dementia: implications for brain protection.Semantic proximity Read ↗

Spotlight on the Pathophysiological Trajectories Linked to Alzheimer’s Disease (AD): Blood-Brain Barrier (BBB); Neuroinflammation; APOE4 Allele and AD- Insulin Resistance (IR) Pathogenic LinkSemantic proximity Read ↗

Navigation Between Alzheimer’s Disease (AD) and Its Various Pathophysiological Trajectories: The Pathogenic Link to Neuroimmunology—Genetics and NeuroinflammationSemantic proximity Read ↗

Research progress on the role and mechanism of blood-brain barrier dysfunction in Alzheimer's diseaseSemantic proximity Read ↗

Interrelationship between Alzheimer's disease and cardiac dysfunction: the brain-heart continuum?Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.