TY - JOUR
T1 - Microbes and Alzheimer's Disease
AU - Itzhaki, Ruth F.
AU - Lathe, Richard
AU - Balin, Brian J.
AU - Ball, Melvyn J.
AU - Bearer, Elaine L.
AU - Braak, Heiko
AU - Bullido, Maria J.
AU - Carter, Chris
AU - Clerici, Mario
AU - Cosby, S. Louise
AU - Del Tredici, Kelly
AU - Field, Hugh
AU - Fulop, Tamas
AU - Grassi, Claudio
AU - Griffin, W. Sue T.
AU - Haas, Jürgen
AU - Hudson, Alan P.
AU - Kamer, Angela R.
AU - Kell, Douglas B.
AU - Licastro, Federico
AU - Letenneur, Luc
AU - Lövheim, Hugo
AU - Mancuso, Roberta
AU - Miklossy, Judith
AU - Otth, Carola
AU - Palamara, Anna Teresa
AU - Perry, George
AU - Preston, Christopher
AU - Pretorius, Etheresia
AU - Strandberg, Timo
AU - Tabet, Naji
AU - Taylor-Robinson, Simon D.
AU - Whittum-Hudson, Judith A.
PY - 2016
Y1 - 2016
N2 - We are researchers and clinicians working on Alzheimer’s disease (AD) or related topics, and we write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest AD progression.
We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain, notably herpes simplex virus type 1 (HSV1),Chlamydia pneumoniae, and several types of spirochaete, in the etiology of AD [1–4]. Fungal infection of AD brain [5, 6] has also been described, as well as abnormal microbiota in AD patient blood [7]. The first observations of HSV1 in AD brain were reported almost three decades ago [8]. The ever-increasing number of these studies (now about 100 on HSV1 alone) warrants re-evaluation of the infection and AD concept.
AD is associated with neuronal loss and progressive synaptic dysfunction, accompanied by the deposition of amyloid- (A) peptide, a cleavage
product of the amyloid- protein precursor (APP), and abnormal forms of tau protein, markers that have been used as diagnostic criteria for the disease [9, 10]. These constitute the hallmarks of AD, but whether they are causes of AD or consequences is unknown. We suggest that these are indicators of an infectious etiology. In the case of AD, it is often not realized that microbes can cause chronic as well as acute diseases; that some microbes can remain latent in the body with the potential for reactivation, the effects of which might occur years after initial infection; and that people can be infected but not necessarily affected, such that ‘controls’, even if infected, are asymptomatic [2].
AB - We are researchers and clinicians working on Alzheimer’s disease (AD) or related topics, and we write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest AD progression.
We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain, notably herpes simplex virus type 1 (HSV1),Chlamydia pneumoniae, and several types of spirochaete, in the etiology of AD [1–4]. Fungal infection of AD brain [5, 6] has also been described, as well as abnormal microbiota in AD patient blood [7]. The first observations of HSV1 in AD brain were reported almost three decades ago [8]. The ever-increasing number of these studies (now about 100 on HSV1 alone) warrants re-evaluation of the infection and AD concept.
AD is associated with neuronal loss and progressive synaptic dysfunction, accompanied by the deposition of amyloid- (A) peptide, a cleavage
product of the amyloid- protein precursor (APP), and abnormal forms of tau protein, markers that have been used as diagnostic criteria for the disease [9, 10]. These constitute the hallmarks of AD, but whether they are causes of AD or consequences is unknown. We suggest that these are indicators of an infectious etiology. In the case of AD, it is often not realized that microbes can cause chronic as well as acute diseases; that some microbes can remain latent in the body with the potential for reactivation, the effects of which might occur years after initial infection; and that people can be infected but not necessarily affected, such that ‘controls’, even if infected, are asymptomatic [2].
KW - ALZEHEIMER'S DISEASE
KW - ALZEHEIMER'S DISEASE
UR - http://hdl.handle.net/10807/75908
U2 - 10.3233/JAD-160152
DO - 10.3233/JAD-160152
M3 - Article
SN - 1387-2877
VL - 51
SP - 979
EP - 984
JO - Journal of Alzheimer's Disease
JF - Journal of Alzheimer's Disease
ER -