This study states that Alzheimer’s illness (AD) is described by two primary neuropathological trademarks—amyloid beta (Aβ) plaques and tau neurofibrillary tangles. Albeit the pathogenic instruments of AD stay indistinct, a few examinations uncovered mitochondrial shortfalls at early sickness stages1 and furthermore in preclinical models.2, 3 The mitochondrial course speculation recommends that the underlying decrease in mitochondrial work triggers synaptic misfortune and changes in tau and Aβ homeostasis.4 likewise, developing proof additionally involves autophagic and lysosomal irregularities in the pathogenesis of AD.5-7 This is went with and maybe further exasperated by supported autophagy enlistment, which ultimately overburdens lysosomal limits in neurons.8 Moreover, impeded autophagic transition builds Aβ discharge and plaque formation9, 10 just as levels of divided andhyperphosphorylated tau (p‐tau).
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 fragmented degradation.14 Although every now and again 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 likewise present in other cerebrum areas and in different neurodegenerative disorders.
Reference link- https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.12212
