The present disclosure is directed to a multi-species prion protein or peptide thereof, and vaccine compositions comprising the same that are useful for the vaccination and treatment of mammalian subjects at risk of having or having prion disease. Also disclosed herein are isolated proteins and peptides, polymers, vaccines, animal bait or feed, antibodies, and methods of inhibiting the onset of or treating a prion disease.

A method of treating a synucleinopathy with a peptide

TABLE-US-00001 (C)DQPVLPD (SEQ ID NO: 59), (C)DMPVLPD (SEQ ID NO: 60), (C)DSPVLPD (SEQ ID NO: 61), (C)DQPVLPDN (SEQ ID NO: 64), (C)DMPVLPDN (SEQ ID NO: 65), (C)DSPVLPDN (SEQ ID NO: 66), (C)HDRPVTPD (SEQ ID NO: 70), (C)DRPVTPD (SEQ ID NO: 71), (C)DVPVLPD (SEQ ID NO: 72), (C)DTPVYPD (SEQ ID NO: 73), (C)DTPVIPD (SEQ ID NO: 74), (C)HDRPVTPDN (SEQ ID NO: 75), (C)DRPVTPDN (SEQ ID NO: 76), (C)DVPVLPDN (SEQ ID NO: 78), (C)DTPVYPDN (SEQ ID NO: 79), (C)DQPVLPDG (SEQ ID NO: 81), (C)DMPVLPDG (SEQ ID NO: 82), (C)DSPVLPDG (SEQ ID NO: 83), (C)DHPVHPDS (SEQ ID NO: 86), (C)DMPVSPDR (SEQ ID NO: 87), (C)DRPVYPDI (SEQ ID NO: 90), (C)DHPVTPDR (SEQ ID NO: 91), (C)DTPVLPDS (SEQ ID NO: 93), (C)DMPVTPDT (SEQ ID NO: 94), (C)DAPVTPDT (SEQ ID NO: 95), (C)DSPWPDN (SEQ ID NO: 96), (C)DLPVTPDR (SEQ ID NO: 97), (C)DSPVHPDT (SEQ ID NO: 98), (C)DAPVRPDS (SEQ ID NO: 99), (C)DMPVWPDG (SEQ ID NO: 100), (C)DRPVQPDR (SEQ ID NO: 102), (C)YDRPVQPDR (SEQ ID NO: 103), (C)DMPVDADN (SEQ ID NO: 105), DQPVLPD(C) (SEQ ID NO: 106), and DMPVLPD(C) (SEQ ID NO: 107.

Methods for inducing anti-phosphorylated Tau antibodies without inducing a severe adverse event in humans are described. The methods include administering to the subject an effective amount of liposomes including a toll-like receptor 4 agonist and a Tau phosphopeptide presented on the surface of the liposome.

The invention provides improved agents and methods for treatment of diseases associated with synucleinopathic diseases, including Lewy bodies of alpha-synuclein in the brain of a patient. Such methods entail administering agents that induce a beneficial immunogenic response against the Lewy body. The methods are particularly useful prophylactic and therapeutic treatment of Parkinson's disease.

The present invention is directed to pharmaceutical agents and compositions useful for the treatment and prevention of amyloid disease in a subject. The invention further relates to isolated antibodies that recognize a common conformational epitope of amyloidogenic proteins or peptides that are useful for the diagnosis, treatment, and prevention of amyloid disease.

The disclosure provides peptide compositions and immunotherapy compositions comprising an amyloid-beta (Aβ) peptide and a fau. peptide. The disclosure also provides methods of treating or effecting prophylaxis of Alzheimer's disease or oilier diseases with beta-amyloid deposition in a subject, including methods of clearing deposits, inhibiting or reducing aggregation of Aβ and/or tan, blocking the uptake by neurons, clearing amyloid, and inhibiting propagation of tau seeds in a subject having or at risk of developing Alzheimer's disease or other diseases containing tau and/or amyloid-beta accumulations. The methods include administering to such patients the compositions comprising an amyloid-beta (Aβ) peptide and a tau peptide.

The present invention relates to virus-like particles of plant virus Cucumber Mosaic Virus (CMV), and in particular to modified VLPs of CMV comprising Th cell epitopes, in particular universal Th cell epitopes. Furthermore, these modified VLPs serve as, preferably, vaccine platform, for generating immune responses, in particular antibody responses, against antigens linked to said modified VLPs. The presence of the Th cell epitopes, in particular universal Th cell epitopes, led to a further increase in the generated immune response.

Traumatic brain injury (TBI) is a leading cause of mortality and morbidity around the world. Active immunization with GFAP protein or GFAP peptide or passive immunization with anti-GFAP antibodies or treatment with a GFAP-binding aptamer can be used to reduce the post-TBI induced expression of GFAP, Tau and p-Tau in brain cortex tissues to attenuate the increased serum levels of GFAP after brain injury, and reduce the serum levels of pNF-H, Tau and p-Tau TBI. In addition, GFAP immunization can alleviate anxiety behavior and improve cognitive performance post-injury. Thus, active or passive GFAP immunization or administration of GFAP-binding aptamer(s) provides a treatment with therapeutic value in suppressing astroglial activation/astrogliosis, and in treating neural injuries such as traumatic brain injury, stroke, spinal cord injury, cerebral hemorrhage, or neurodegenerative diseases such as chronic traumatic encephalopathy, Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis, amyotrophic lateral sclerosis, frontotemporal dementia, and other dementias.

Disclosed are immunogenic peptides of the HTT protein and HTT specific antibodies for use in the prevention and/or treatment of Huntington's disease.

Methods and compositions for treating central nervous system diseases and disorders are disclosed.