Science

Ruth F. Itzhakia, Richard Latheb, Brian J. Balin, Melvyn J. Ball, Elaine L. Bearer, Heiko Braak, Maria J. Bullido, Chris Carter, Mario Clerici, S. Louise Cosby, Kelly Del Tredici, Hugh Field, Tamas Fulop, Claudio Grassi, W. Sue T. Griffin, Jürgen Haas, Alan P. Hudson, Angela R. Kamer, Douglas B. Kell, Federico Licastro, Luc Letenneur, Hugo Lövheim, Roberta Mancuso, Judith Miklossy, Carola Otth, Anna Teresa Palamara, George Perry, Christopher Preston, Etheresia Pretoriusa, Timo Strandbergb, Naji Tabetc, Simon D. Taylor-Robinsond, and Judith A. Whittum-Hudson

Ruth F. Itzhakia, Richard Latheb, Brian J. Balin, Melvyn J. Ball, Elaine L. Bearer, Heiko Braak, Maria J. Bullido, Chris Carter, Mario Clerici, S. Louise Cosby, Kelly Del Tredici, Hugh Field, Tamas Fulop, Claudio Grassi, W. Sue T. Griffin, Jürgen Haas, Alan P. Hudson, Angela R. Kamer, Douglas B. Kell, Federico Licastro, Luc Letenneur, Hugo Lövheim, Roberta Mancuso, Judith Miklossy, Carola Otth, Anna Teresa Palamara, George Perry, Christopher Preston, Etheresia Pretoriusa, Timo Strandbergb, Naji Tabetc, Simon D. Taylor-Robinsond, and Judith A. Whittum-Hudson
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. Fungal infection of AD brain has also been described, as well as abnormal microbiota in AD patient blood. The first observations of HSV1 in AD brain were reported almost three decades ago. 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-β (Aβ) peptide, a cleavage product of the amyloid-β protein precursor (AβPP), and abnormal forms of tau protein, markers that have been used as diagnostic criteria for the disease. 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