• following injection of LPS into the substantia nigra

• following injection of LPS into the substantia nigra, mice exhibit an increased loss of dopaminergic neurons that is associated with insoluble and aggregated SNCA compared to in Snca^tm1Rosl Tg(Prnp-SNCA)7Vle and Snca^tm1Rosl homozygotes

• however, loss of dopamine neurons is not due to an abnormal inflammatory response following injection of LPS into the substantia nigra

• following injection of LPS into the substantia nigra, mice exhibit an increased loss of dopaminergic neurons compared to in Snca^tm1Rosl Tg(Prnp-SNCA)7Vle and Snca^tm1Rosl homozygotes

• by 8 months of age, begin to lose weight

• over time become unable to feed themselves

• by 8 months of age, grooming is neglected

• unable to right themselves when placed on their sides

• temulous motion is seen in some mice, possibly related to attempted muscular activity

• eventually are unable to stand up and support their own body weight

• develop hunched backs by 8 months of age

• by 8 months of age, exhibit severe movement impairment with resistance to passive movement and partial paralysis of limbs, accompanied by periods of freezing of hindlimb

• reduced ambulation by 8 months of age

• partial paralysis of limbs is observed by 8 months of age, beginning at a hindleg but affecting all limbs within a few days

• astrocytic gliosis

• endoneurial space is increased and axons are filled with vacuoles in the ventral roots of aged mice

• develop age-dependent intracytoplasmic neuronal alpha-synuclein inclusions that contain 10-16 nm wide fibrils similar to those seen in human alpha-synucleinopathies, with dense accumulation in the spinal cord, brainstem, cerebellum, and thalamus

• following axonal degeneration, the myelin sheath loosens and unravels

• show signs of neurodegeneration by 8 months of age and develop neurodegenerative disease within 16 months of age

• significant axonal degeneration in aged mice

• exhibit sparse neurogenic muscle atrophy

• develop the severe and complex motor impairment leading to paralysis and death that is seen in homozygous transgenics, however onset is delayed from 16 months of age to 22-28 months of age

• develop a similar neurodegenerative disease that is observed in homozygous transgenic mice, however onset is delayed from 16 months of age to 22-28 months of age