DR. ELIEZER MASLIAH, M.D.
Medical Practice at Arbor Dr, San Diego, CA

7393994, Jul 1, 2008

Aug 20, 2001

09/933640

Eliezer Masliah - San Diego CA, US
Edward Rockenstein - Chula Vista CA, US
Margaret E. Mallory - Encinitas CA, US

Regents of the University of California - Oakland CA

G01N 33/00, A01K 67/027

800 3, 800 18

Alzheimer's disease, Parkinson's disease and Lewy body disease are the most commonly found neurodegenerative disorders in the elderly. The invention is a transgenic mouse that contains two transgenes, human α-synuclein and human amyloid precursor protein, which are responsible for the formation of the neuritic plaques, Lewy bodies and neurodegeneration seen in the above mentioned diseases. The transgenic mouse is an accurate model for disease by both functional and pathological assays.

2011022, Sep 15, 2011

Sep 29, 2009

13/119400

Eliezer Masliah - San Diego CA, US
Brian Spencer - San Diego CA, US
Edward Rockenstein - Chula Vista CA, US
Robert Marr - North Chicago IL, US

THE REGENTS OF THE UNIVERSITY OF CALIFORNIA - Oakland CA
ROSALIND FRANKLIN UNIVERSITY OF MEDICINE AND SCIENCE - North Chicago IL

A61K 9/127, C12N 9/96, A61K 38/54, A61P 25/16, A61P 25/28, A61P 25/00, C12N 5/02, B82Y 5/00

424450, 435188, 424 943, 435375, 977773

The invention provides compositions for increasing the clearance of protein aggregates, and pharmaceutical compositions comprising them, and methods for making and using them, including methods for accelerating protein aggregate clearance in the CNS, e.g., for treating diseases that are characterized by protein aggregation—including some degenerative neurological diseases such as Parkinson's disease. In one aspect, the compositions of the invention specifically target synuclein, beta-amyloid and/or tau protein aggregates, and the methods of the invention can be used to specifically prevent, reverse, slow or inhibit synuclein, beta-amyloid and/or tau protein aggregation. In alternative embodiments, the compositions and methods of the invention, are used to treat, prevent, reverse (partially or completely) or ameliorate (including slowing the progression of) degenerative neurological diseases related to or caused by protein aggregation, e.g., synuclein, beta-amyloid and/or tau protein aggregation. In one aspect, compositions and methods of this invention are used to treat, prevent or ameliorate (including slowing the progression of) Parkinson's disease, fronto-temporal dementia (FTD), Alzheimer's Disease (AD), Lewy body disease (LBD) and Multiple system atrophy (MSA).

7459601, Dec 2, 2008

May 24, 2004

10/853774

Eliezer Masliah - San Diego CA, US
Makoto Hashimoto - La Jolla CA, US
Edward Rockenstein - Chula Vista CA, US
Lennart Mucke - San Francisco CA, US

The Regents of the University of California - Oakland CA

A01K 67/00, A01K 67/033, A01K 67/027, C12N 5/06, C12N 5/10

800 12, 800 18, 435354

In methods for screening treatments for, and treatment of, neurodegenerative diseases, aggregation in neurons of NACP/α-synuclein is measured and expression of a non-amyloidogenic protein is stimulated in order to reduce the level aggregration. For purposes of screening agents for treatment of neurodegenerative disease, oxidative stress in the neuronal cells is stimulated by introducing a mixture of metal-ions and hydrogen peroxide. Examples of appropriate metals include iron, aluminum, and copper. After introduction of the agent under evaluation for stimulation of expression of non-amyloidogenic protein, the effectiveness is measured by testing for a decrease in the level of aggregation of NACP/α-synuclein. In an exemplary embodiment, the non-amyloidogenic protein is β-synuclein. The aggregation of NACP/α-synuclein is dependent upon the concentration of metal ions in the neuronal cells.

7276643, Oct 2, 2007

Feb 20, 2001

10/204337

Eliezer Masliah - San Diego CA, US
Edward Rockenstein - Chula Vista CA, US
Hersey Mallory, legal representative - Encinitas CA, US

The Regents of the University of California - Oakland CA

A01K 67/027, G01N 33/00, C12N 5/02

800 18, 800 3, 435325

The methodologies of the present invention demonstrate that a critical balance between pro- and anti-amyloidogenic molecules exists that regulates amyloid formation and cell death in Alzheimer's disease and Parkinson's disease. β-Synuclein, the non-amyloidogenic homologue of α-synuclein, is a negative modulator of α-synuclein and Aβ aggregation, having neuroprotective properties against α-synuclein and Aβ neurotoxicity and that β-synuclein and therapeutic agents derived therefrom block amyloidogenesis and neurodegeneration in vivo. The method of the present invention establishes that β-synuclein blocks Aβ aggregation either by direct inhibition of Aβ amyloidogenesis or indirectly via either α-synuclein or its 35 a. a. NAC region, inferring neuroprotective characteristics within the effected cells. The generation of a transgenic mouse line and a cell system overexpressing α-synuclein characterizes the mechanisms by which β-synuclein blocks α-synuclein and Aβ aggregation and that this mechanism offers protection to the cell against amyloid formation as seen in the pathologies of Alzheimer's disease and Parkinson's disease.

7727957, Jun 1, 2010

Oct 31, 2003

10/699517

Dale B. Schenk - Burlingame CA, US
Eliezer Masliah - San Diego CA, US

Janssen Alzheimer Immunotherapy - Little Island, County Cork
The Regents Of The University Of California - Oakland CA

A61K 38/17, A61K 39/395, A61K 39/00, A61K 39/385

514 12, 4241301, 4241851, 4241931, 4242781

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 for prophylactic and therapeutic treatment of Parkinson's disease.

2011013, Jun 9, 2011

Mar 23, 2010

12/729902

Dale B. Schenk - Burlingame CA, US
Eliezer Masliah - San Diego CA, US

JANSSEN ALZHEIMER IMMUNOTHERAPY - LITTLE ISLAND
THE REGENTS OF THE UNIVERSITY OF CALIFORNIA - OAKLAND CA

A61K 39/395, A61K 39/00, A61K 39/385, A61P 37/04, A61P 25/00

4241721, 4241841, 4241931

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 for prophylactic and therapeutic treatment of Parkinson's disease.

2010003, Feb 4, 2010

Aug 9, 2005

11/660015

Dale B Schenk - Burlingame CA, US
Eliezer Masliah - San Diego CA, US
Manuel J. Buttini - Emeryville CA, US
Tamie J. Chilcote - San Francisco CA, US
Edward Rockenstein - Chula Vista CA, US
Kate Dora Games - Belmont CA, US

ELAN PHARMACEUTICALS, INC. - SAN FRANCISCO CA

A61K 49/00, A61K 39/395, C07K 16/18, C12N 5/16, A61K 39/00, A61P 25/28

800 3, 4241391, 4241451, 4241331, 5303889, 435326, 4241781

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 for prophylactic and therapeutic treatment of Parkinson's disease.

2005003, Feb 17, 2005

Aug 9, 2004

10/915214

Dale Schenk - Burlingame CA, US
Eliezer Masliah - San Diego CA, US

Elan Pharmaceuticals, Inc. - So. San Francisco CA
The Regents of the University of California - Oakland CA

A61K039/00, A61K038/17

424185100, 514012000

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 for prophylactic and therapeutic treatment of Parkinson's disease.