Challenges and directions for the pathogen hypothesis of Alzheimer’s disease

  title={Challenges and directions for the pathogen hypothesis of Alzheimer’s disease},
  author={Stephen R. Robinson and Curtis B Dobson and Joseph M. Lyons},
  journal={Neurobiology of Aging},
Pathogens as a cause of Alzheimer’s disease
Alzheimer ' s disease and the role of infectious Agents : A review
It is suggested that some infectious agents, may contribute to the pathogenesis of AD and with the prevention and treatment of such infectious agents the sanitation authorities can decrease the risk of AD.
Role of Infection in the Pathogenesis of Alzheimer’s Disease
This work has shown that peripheral infections may have a role to play in accelerating neurodegeneration in Alzheimer’s disease by activating already primed microglial cells within the CNS.
Is Alzheimer's disease an infectious neurological disease? A review of the literature.
An overview of new findings around the relationship between microorganisms and AD, challenges facing the validity of the theory, and recommendations on how the scientific community can best develop alternative approaches to address the pathophysiology of AD are provided.
Chlamydophila pneumoniae Infection and Its Role in Neurological Disorders
The demonstration of C. pneumoniae by histopathological, molecular and culture techniques in the late-onset AD dementia has suggested a relationship between CNS infection with C. tuberculosis and the AD neuropathogenesis, and the role of Chlamydia in the pathogenesis of mental or neurobehavioral disorders including schizophrenia and autism is uncertain and fragmentary and will require further confirmation.
Association of Alzheimer's disease and Chlamydophila pneumoniae.
Anti-Viral Properties of Amyloid-β Peptides.
The data that support the interpretation that A β peptides behave as AMP are reviewed, with an emphasis on studies concerning HSV-1 and a putative molecular mechanism that suggests that interactions between Aβ peptides and the HSv-1 fusogenic protein gB lead to impairment of HSVs infectivity by preventing the virus from fusing with the plasma membrane.
Alzheimer's Amyloid-β is an Antimicrobial Peptide: A Review of the Evidence.
The antimicrobial role of Aβ may explain why increased rates of infection have been observed in some of the AD clinical trials that depleted Aβ, and progress toward a cure for AD will accelerate once treatment strategies begin to take into account the likely physiological functions of this enigmatic peptide.


Herpes simplex virus type 1 and Alzheimer’s disease
Human herpes virus infections and Alzheimer's disease
No evidence of viral RNA in the central nervous system (CNS) of demented individuals with extensive neuropathological changes of AD is found, solving one problem in testing the viral hypothesis of causation, i.e. the sensitivity of the methods used in the search for latent infection.
Herpes simplex encephalitis: involvement of apolipoprotein E genotype.
It seems that apoE ε2 is a risk factor for HSE, based on the allele frequencies obtained from specimens from the brain or spleen of patients with HSE.
Identification and localization of Chlamydia pneumoniae in the Alzheimer's brain
C. pneumoniae is present, viable, and transcriptionally active in areas of neuropathology in the AD brain, possibly suggesting that infection with the organism is a risk factor for late-onset Alzheimer's disease.
Viral infections of the CNS with special emphasis on herpes simplex infections
A combination therapy with acyclovir plus prednisone seems to be indicated in a patient with Bell's palsy, if other causes for the clinical/neurological syndrome of peripheral facial palsy have been excluded, and a large scale prospective randomised double blind study is confirmed.
Viral encephalitis: familiar infections and emerging pathogens
Neurological disease and herpes simplex virus
Only two patients with Alzheimer's disease showed areas of brain positive for HSV antigen (VA), which suggests “coincidental disease” processes within these two patients and means that any hypothesis implicating HSV as an aetiological agent in degenerative disease must still remain extremely speculative.
Systemic infection, interleukin 1β, and cognitive decline in Alzheimer’s disease
This prospective pilot study in Alzheimer's disease subjects showed that cognitive function can be impaired for at least two months after the resolution of a systemic infection and that cognitive impairment is preceded by raised serum levels of interleukin 1β.