Could COVID-19 anosmia and olfactory dysfunction trigger an increased risk of future dementia in patients with ApoE4?

Anosmia – The common missing link between Alzheimer’s disease and COVID-19

“…Apart from the other noted reasons of AD such as deposition of Amyloid Beta (A) plaques and Neurofi brillary Tangles (NFT), hyperactivity of acetyl choline esterase, genetic predisposition and involvement of proteomics, a novel approach in diagnosing AD pathogenesis seems to be the "anosmia" [2,4]. This notion is substantiated by the fact that people carrying e4 allelle of apo-lipoprotein E4 (Apo E4) are https://www.peertechzpublications.com/journals/annals-of-alzheimer-s-and-dementia-care Citation: Rahman at increased risk of developing AD as well as anosmia [5]. As aging progresses, A and NFT accumulate in neurons of the hippocampus and entorhinal cortex that disrupt olfaction as well as memory and learning processes ultimately leading towards AD complications especially dementia [2][3][4][5].…”

“…This notion is substantiated by the fact that people carrying e4 allelle of apo-lipoprotein E4 (Apo E4) are https://www.peertechzpublications.com/journals/annals-of-alzheimer-s-and-dementia-care Citation: Rahman at increased risk of developing AD as well as anosmia [5]. As aging progresses, A and NFT accumulate in neurons of the hippocampus and entorhinal cortex that disrupt olfaction as well as memory and learning processes ultimately leading towards AD complications especially dementia [2][3][4][5]. Older people (aged 57-85 years) having hyposmia (reduced ability of smelling) bears two times increased risk of developing dementia within fi ve years than their age matched controls [6,7].…”

Anosmia – The Missing and Common Link Between Alzheimer’s Disease and Covid-19

“…Apart from the other noted reasons of AD such as deposition of amyloid beta (Aβ) plaques and neurofibrillary tangles (NFT), hyperactivity of acetyl choline esterase, genetic predisposition and involvement of proteomics, a novel approach in diagnosing AD pathogenesis seems to be the "anosmia" [2][3][4]. This notion is substantiated by the fact that people carrying e4 allelle of apo-lipoprotein E4 (Apo E4) are at increased risk of developing AD as well as anosmia [5]. As aging progresses, Aβ and NFT accumulate in neurons of the hippocampus and entorhinal cortex that disrupt olfaction as well as memory and learning processes ultimately leading towards AD complications especially dementia [2][3][4][5].…”

“…This notion is substantiated by the fact that people carrying e4 allelle of apo-lipoprotein E4 (Apo E4) are at increased risk of developing AD as well as anosmia [5]. As aging progresses, Aβ and NFT accumulate in neurons of the hippocampus and entorhinal cortex that disrupt olfaction as well as memory and learning processes ultimately leading towards AD complications especially dementia [2][3][4][5]. Older people (aged 57-85 years) having hyposmia (reduced ability of smelling) bears two times increased risk of developing dementia within five years than their age matched controls [6][7].…”

Survivors of SARS-CoV-2 Infection Show Neuropsychiatric Sequelae Measured by Surveys, Neurocognitive Testing, and Magnetic Resonance Imaging: Preliminary Results

“…A recent meta-analysis suggests abnormalities in the olfactory bulb are the most common structural neuroimaging findings following COVID-19 infection 19 . Furthermore, structural abnormalities in the olfactory bulb have been associated with anosmia (a partial or complete loss of smell) 20,21 , and there has been speculation in the literature that olfactory dysfunction in COVID-19 may increase risk of future dementia 22 .…”