Alzheimer's disease

  title={Alzheimer's disease},
  author={Colin L. Masters and Randall J. Bateman and Kaj Blennow and Christopher C. Rowe and Reisa A. Sperling and Jeffrey L. Cummings},
  journal={Nature Reviews Disease Primers},
Alzheimer's disease is a chronic illness with long preclinical and prodromal phases (20 years) and an average clinical duration of 8–10 years. The disease has an estimated prevalence of 10–30% in the population >65 years of age with an incidence of 1–3%. Most patients with Alzheimer's disease (>95%) have the sporadic form, which is characterized by a late onset (80–90 years of age), and is the consequence of the failure to clear the amyloid-β (Aβ) peptide from the interstices of the brain. A… 

The neuropathological diagnosis of Alzheimer’s disease

This review outlines etiologically-linked pathologic features of Alzheimer's disease, as well as those that are inevitable findings of uncertain significance, such as granulovacuolar degeneration and Hirano bodies.

Can mouse models mimic sporadic Alzheimer’s disease?

The current situation regarding AD mouse models, and the problems to develop a sporadic mouse model of AD are discussed.

Patient-Derived Fibroblasts With Presenilin-1 Mutations, That Model Aspects of Alzheimer’s Disease Pathology, Constitute a Potential Object for Early Diagnosis

Fibroblasts from patients with FAD-PS1 present alterations in signaling pathways related to cellular stress, autophagy, lysosomes, and tau phosphorylation, which can be useful in modeling pathwaysrelated to neurodegeneration, as well as for the identification of early AD biomarkers.

Methodological Issues in Randomized Clinical Trials for Prodromal Alzheimer's and Parkinson's Disease

Some of the methodological challenges in the design of trials for pre-clinical and prodromal phases of AD and PD are discussed, to critically review the recent studies, and to discuss methodological approaches to mitigate these challenges in trial design.

Improvements of symptoms of Alzheimer`s disease by inhibition of the angiotensin system.

Genetic Variability in Molecular Pathways Implicated in Alzheimer's Disease: A Comprehensive Review

Gene clustering into molecular pathways can provide background for identification of novel molecular targets and may support the development of tailored and personalized treatment of AD.

A metabolic perspective of late onset Alzheimer's disease.

Alzheimer’s Disease and Vascular Aging

Vascular and Metabolic Factors in Alzheimer’s Disease and Related Dementias: Introduction

  • C. Iadecola
  • Medicine, Biology
    Cellular and Molecular Neurobiology
  • 2015
Evidence indicates that mixed AD-vascular dementia the most common cause of cognitive impairment in the aged and epidemiological studies have indicated that clinically diagnosed AD and VCI share common risk factors, such as hypertension, obesity, diabetes, etc., suggesting the involvement of common pathogenic factors.

Cerebrospinal fluid biomarkers for understanding multiple aspects of Alzheimer’s disease pathogenesis

Looking into the multifactorial nature of AD and the overlapping pathology with other forms of dementia, it is important to integrate the core CSF biomarkers with a broader panel of other biomarkers reflecting different aspects of pathology.



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The strong protective effect of the A673T substitution against Alzheimer’s disease provides proof of principle for the hypothesis that reducing the β-cleavage of APP may protect against the disease.

Biology of Aβ Amyloid in Alzheimer's Disease

Three of the genes which are now known to be linked to AD, including PS1, beta PP, and apoE, have been established immunohistochemically and biochemically to be components of senile plaques and current data suggest that new therapeutic approaches which may inhibit the aggregation and/or the conformational change of sA beta to A beta fibrils have the greatest likelihood to make a significant impact on controlling amyloid accumulation in AD.

Decreased Clearance of CNS β-Amyloid in Alzheimer’s Disease

The common late-onset form of Alzheimer's disease is characterized by an overall impairment in Aβ clearance, and both Aβ42 and Aβ40 production and clearance rates were impaired in Alzheimer’s disease compared with controls.

Short-term clinical outcomes for stages of NIA-AA preclinical Alzheimer disease

Despite the short follow-up period, operationalization of the new preclinical AD recommendations confirmed that advancing preclinical stage led to higher proportions of subjects who progressed to MCI or dementia.

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Evidence that the presenilin proteins, mutations in which cause the most aggressive form of inherited AD, lead to altered intramembranous cleavage of the beta-amyloid precursor protein by the protease called gamma-secretase has spurred progress toward novel therapeutics and provided discrete biochemical targets for drug screening and development.

Hippocampal sclerosis in advanced age: clinical and pathological features.

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Biochemical markers in persons with preclinical familial Alzheimer disease

The finding of elevated F2-isoprostane levels in the CSF of preclinical FAD MCs suggests that oxidative stress occurs downstream to mismetabolism of amyloid precursor protein.