The main objective of this review is to prove how Alzheimer’s illness (AD) is portrayed by two principle neuropathological trademarks—amyloid beta (Aβ) plaques and tau neurofibrillary tangles. Albeit the pathogenic components of AD stay hazy, a few investigations uncovered mitochondrial deficiencies at early illness stages1 and furthermore in preclinical models.2, 3 The mitochondrial course theory recommends that the underlying decrease in mitochondrial work triggers synaptic misfortune and changes in tau and Aβ homeostasis.4 likewise, developing proof additionally embroils autophagic and lysosomal irregularities in the pathogenesis of AD.5-7 This is went with and maybe further bothered by supported autophagy enlistment, which in the end overburdens lysosomal limits in neurons.8 Moreover, weakened autophagic transition builds Aβ emission and plaque formation9, 10 just as levels of divided andhyperphosphorylated tau (p‐tau).11, 12
Another well‐documented yet inadequately comprehended neuropathological highlight of AD is granulovacuolar degeneration (GVD). These intraneuronal gatherings of enormous twofold layer bound vacuoles holding a focal granule13 are believed to be late‐stage autophagic leftovers of inadequate degradation.14 Although regularly found in ordinary maturing, GVD bodies (GVBs) in patients with AD well surpass age‐matched controls.15 Most noticeably situated in hippocampal pyramidal neurons, GVBs are additionally present in other cerebrum districts and in different neurodegenerative disorders.
Reference link- https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.12198
